final Flashcards
active immunity
body is exposed to pathogen and produces its own antibodies (natural: infection, artificial: vaccination)
passive immunity
occurs when we acquire antibodies made my another organism
natural: placenta, breast milk, artificial: gamma globulins, faster and does not generate memory
constant region
on the main tail - determines the mechanism used to destroy the antigen, structural framework, same on the antibody
Fab
the light chain on the tails - the binding fragment - recognizes the antigen, consists of two variable and two constant domains
Fc
he main tail, crystallizable fragment - interacts with other elements of the immune system such as phagocytes or components of the complement pathway to promote removal of the antigen
variable region
on the two tails, antigen specificity of the antibody, binds to the antigen, divalent
IgM
pentamer, associated with primary response, strongly activates the complements, naive B cells, micro heavy chain
IgG
monomer, most abundant isotype in the serum, longest half life (23 days), 4 subclasses (IgG1-4), most IgG cross the placenta (FcRB), opsonin (Fc receptor fetus to placenta), activates complements gamma heavy chain
IgA
mono to tetramer, in external excretions (saliva, intestinal and bronchial mucus, breast milk) alpha chain
IgE
monomer, target parasites and allergen, decorate mast cells, basophils, and eosinophils through FcR, causing degranulation, transportation relies on the Fc fragment
IgD
appear on the surface of B cells, the role is unclear
five physiological functions of antibodies
- antigen clumping (valence) and neutralization
- opsonization
- ADCC
- complement fixation
antigen clumping and neutralization
toxins, control infection, targets of the therapeutic antibodies
opsonization
neutrophils and macrophages *FCgama, IGg - opsonin an antibody or other substance which binds to foreign microorganisms or cells making them more susceptible to phagocytosis.
ADCC
through degranulation of mast cells, basophils, eosinophils and NK (IgE, IgG) - antibody-dependent cell-mediated cytotoxicity, is a mechanism of cell-mediated immune defense whereby an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies.
complement fixation
C3b (potent in opsonization: tagging pathogens, immune complexes (antigen-antibody), and apoptotic cells for phagocytosis) opsonization, degranulation, chemotaxis, MAC (membrane attack complex) (IgM, IgG) - the process of binding serum complement to the product formed by the union of an antibody and the antigen for which it is specific that occurs when complement is added to a suitable mixture of such an antibody and antigen
primary immune response
clonal selection - plasma membrane of naive B cells, IgA, IgB heterodimer to form BCR, BCR binds to specific antigen leading to receptor oligomerization, specific clone of the B cells proliferates, specific clone of the B cell proliferates and differentiates into IgM secreting plasma membranes and memory B cells, activated B cells can undergo isotope switching and differentiate into plasma cells (IgG, Iga, IgE corresponding memory B cells
secondary response
memory cells encounter the same antigen, rapid clonal expansion to effector to effector cells, differentiation into isotope plasma cells, antibody production and secretion, secondary response is faster and stronger
MHC class I
expressed on all nuceated human cells and recognized by cytotoxic t cells - CD8 binding- B2 microglobulin, cytotoxic T cell attack the virus-infected cells
MHC class II
expressed on all antigen-presenting cells (macrophages, B cells, dendritic cells) recognized by helper T cells - CD4 binding, attacks the antigen presenting cells
cTcells attack cells expressing antigen through MHC-I
release pore-forming perforins, release granzymes that activate apoptotic cascade, activate d
helper tcells enhance immunity
secrete cytokines that activate other immune cells (IFNgamma (TH1) interleukins (activation of B cells, mast cells and eosinophils: TH2 activation of cytotoxic T cells (TH1) 2. bind to B cells and promote their differentiation into plasma cells and memory B cells (including class switching) - HIV destroys helper T cells
integrated immune response to bacterial infection
inflammation, components of bacterial cell wall can directly activate complement cascade leading to chemotaxis, opsonization and MAC formation, alert adaptive immune response: antibody-mediated if bacteria are extracellular, activation of helper T cells lead to cytokine secretion and increased b cell clonal expansion antibody production and B and helper T memory cell generation, repair
integrated immune response
humoral and cell mediated, innate and antibody mediated defense (cestracellular - body cells are infectd cytotoxic T cells and NK cells activated macrohages also secrete cytokines (IFN), NK cells recognize some infected cells lacking MHC-I and kill them -
antigenic drift
caused by high mutation rate of viruses, antibodies do not recognize mutated proteins on viruses, annual flu shot
bacteria
prokaryotic (no nucleus), DNA genetic material, have own machinery for replication and metabolism, cell wall and often a capsule that protects against immune cells can be killed or growth inhibited by antibiotics
MOA: cell wall destruction inhibit protein translation, bind ribosomes, B-lactam
viruses are particles
obligatory intracellular parasites, contain either DNA or RNA, nucleic acid is enclosed in a protein capsid, enveloped viruses are enclosed in an outer layer of host membrane and viral host/protiens called envelope, inhibted by anitvirals not antibiotics
virus invades the host cell
endocytosis (non-enveloped), virus envelope fuses with host cell membrane
virus nucleic acid takes over
hid out (herpes simplex type 1) incorporate DNA into host DNA, use host cell machinery to make DNA/RNA and proteins
virus is released
non-enveloped virus causes host cell to rupture - the cell lyses in host cell - enveloped virus particles bud off from the surface
name the tree major functions of the immune system
- protects against pathogens and other immunogens
- recognizes and removes abnormal self cells (cancer)
- removes dead or damaged cells : scavenger cells (macrophages)
innate immunity
born, broad specificity, recognizes pathogen associated molecular patterns, fast response: inflammation, red, warm, swollen, pain, cytokine mediated
acquired immunity
adaptive, immune response at specific pathogens, slow first response, memory, cell-mediated vs humoral (hep B vaccination, infusion of Hep B to a newborn baby to a women with hep B)
immunorecognition
how the body distinguishes which pathogen/what is not
immunogen
chemical compound that triggers an immune response
antigen
chemical compounds that interact with products of the adaptive immune response
epitopes
one of the antigenic determinants of an antigen (one antigen can have several)
haptens
some LMW molecules become immunogenic only when linked to a carrier protein- doesn’t mass to elicit immune response
adjuvants
substances that enhance the immunogenicity of an antigen - enhance the capability of an antigen to initiate an immune response, bigger the molecule more likely it can initiate an immune response
2 lines of defense against pathogens
- physical and chemical- epithelia, gastric acidity, gladular secretions
- internal immune response - detection, cell-to-cell communication with pathogen, chemotaxis, recruitment and coordination, destruction or suppression, depends on the cytokine and antibodies
granulocyte
(polymorphonuclear leukocyte) - has granules, multiple nuclei, degranulation to produce chemicalst to treat/kill pathogens, smaller leukocytes, neutrophil, eosinophil, basophil
what are granules
contain inflammatory mediators that can be released in the cytoplasm
neutrophil
first responder to an infection, 50-70% PBL, most abundant peripheral cell lymphocyte, first responder to a site of inflammation, degranulate and release cytokines, cause fever, highly motile, phagocytic cells, engulf pathogens, short lived, only one involved in phagocytosis
pathway of a neutorphil attack
- recognition- cell-surface receptors invading pathogen
- invagination- cell membrane surrounds microbes and engulfs pathogens
- phagosome formation- cellular granules release contents into vacuole; membrane NADPH oxidase activated
- killing of pathogens- respiratory burst results in a generation of reactive oxygen and produces molecules that destroy all pathogens
eosinophil
inflammatory cells that defend against parasitic infections, 1-3% PBL, migrate in response to chemotactic signals, exhibit a metabolic burst when activated, defend against parasites (release NO and cytotoxic enzymes to kill), increase several fold in response to parasitic infections, also activated by allergens - more specialized in parasitic infections
basophil
release histamine, causing inflammation in allergy and antigen reaction, rare in PBL, recruited to injury, have cell surface IgE, triggers degranulation, releases histamine (vasodilation), heparin (anticoagulant), cytokines, important in allergic/parasitic infection,
mast cells
also bind IgE, similar function to basophils except are concentrated in connective tissues of the skin, lungs, GI
agranulocytes
mononuclear leukocytes, null cell/natural killer cell, mature b cell, helper t cell, suppressor t cell, monocytic cell, lymphocytes, dendritic cell
monocytic cell
migrate from the blood stream and becomes macrophages, 1-6% PBL, circulating monocytes migrate out of the blood vessel, become macrophages, take residence in tissues: liver, brain, bones
macrophages are effective phagocytes
® Neutrophils and macrophages are primary phagocytes
® Macrophages are larger and more effective phagocytes
Macrophages also remove old RBC and dead-neutrophils
Macrophages are antigen presenting cells (APC) in acquired immunity - involved in bigger blood cells
lymphocytes
□ B cells: antigen presentation and antibody production and differentiate into plasma cells and memory cells, derived from the bone marrow
□ T cells: defense against intracellular pathogens, cytotoxic T cells(kills cell containing pathogens - cancer cells) and helper T cell (secrete different mediators- immune resistant)
Natural killer cells (NK cells): defense against intracellular pathogens
dendritic cells
not leukocyte, □ Antigen presenting cells in many tissues (langerhan cells in skin)
□ Recognize and caputre antigens
□ Migrate to secondary lympoid tissues
□ Present antigens to lymphocytes
Antigen binding activates lymphocytes so they can proliferate and come into the blood stream to fight that antigen
primary lymphoid tissue
(immune cell formation and maturation)
Thymus (produces T cells)
Bone marrow (produces other blood cells)
secondary lymphoid tissue
(mature immune cells interact with pathogen and initiate response)
Encapsulated:
Spleen
Macrophages encounter pathogens in the blood
Lymph node
Un-encapsulated (or diffuse lymphoid tissues):
Tonsils
Gut-associated lymphoid tissue (GALT)
Clusters of lymphoid tissues
Strategically positioned
three major classes of immune pathologies
- Immunodeficiencies (under-reaction): Primary immunodeficiency - more genetic, Acquired immunodeficiency (AIDS, HIV) Allergy or hypersensitivity (over-reaction), immune system) Autoimmune disease (mis-recognition) E.g. type 1 diabetes, rheumatoid arthritis
airway physical and chemical barrier
mucocilliary clearance, secretions containing lysozyme and immunglobulins (adaptive)
digestive tract physical and chemical barrier
salivary lysozyme and immunoglobin, gastric acid, intestinal immunoglobulin
genitourinary tract physical and chemical barrier
cervical mucus plug
innate leukocytes
neutrophils, eosinophils, basophils, null cell (NK), monocyte (macrophage)
adaptive leukocytes
b cell, helper t cell, suppressor t cell
pathogen-associated molecular patterns
leukocytes can recognize certain molecules unique to microorganisms - lipopolysaccharide on the outer membrane of gram-negative bacteria, cell wall polysaccharide from fungi, double strand RNA from virus
PAMPs bind to
leukocyte patter recognition receptors and activate leukocytes to kill (degranulation) or ingest (phagocytosis)
toll-like receptors (TLR)
single-pass transmembrane proteins expressed ont he membranes of leukocytes and non immune cells, 10 TLR identified in human, varying in immune cell distrubution and PAMP recognition, TLR link innate and adaptive immunity on dendritic cells
imiquimod
topical cream that treats genital warts, actinic keratoses, basal cell carcinoma, activates TLR7, enhances innate immunity through secretion of cytokines, activate langerhan cells and enhance adaptive immunity - activates NK, macrophages and B lymphocytes, treats HPV and anti-tumor, innate and adaptive immunity
chemotaxins
chemicals that attract leukocyts to the site of infection
chemotaxin examples
- bacterial toxins and cell wall components
- products of tissue injury: fibrin and collagen fragments
- chemotactic cytokines: macrophage chemoattractant protein (MCP-1), IL8
extraversion
leaves blood vessel for tissue
pus
live and dead neutrophils and macrophages, tissue fluid, cell debris, and remnants of immune process
neutrophil extravasation facilitated by adhesion molecules
ICAM-1, intracellular adhesion molecule
LFA-1, lymphocyte function- associated antigen 1
leukocyte adhesion deficiency
LAD1 caused by defects in LFA-1 leading to ineffective migration and phagocytosis, recurring bacterial infection, ineffective wound healing, impaired pus formation, and granulocytosis
opsonin
antibodies and plasma proteins that tag particles to be ingested - antibodies bridge the gap between the pathogen and the macrophage to facilitate its elimination
free radical formation during neutrophil phagocytosis
- NADPH to NADP+ by NADPH oxidase makes O2 go to O2-
- combines to make hydrogen peroxide
- makes HOCL to make bacterium
- hydrogen peroxide makes a free radical through iron to bacterum
- iNOS comes from NO
- ONOO- makes bacterium
what do NK cells do
target virus-infected cells and induce apoptosis, act faster than lymphocytes, attack some tumor cells,
how do NK cells recognize virus-infected tumor cells
damaged DAMPs
NK cells and other lymphocytes secrete ____
antiviral cytokines including interferons, these IFNs interfere with viral replication, IFN gamma activates macrophages and other immune cells, IFN can cause fever, muscle pain, flu-like symptoms
three important roles of inflammation
- attracts immune cells and chemical mediators to the site of infection - cytokine
- produces a physical barrier to retard the spread of infection
- promotes tissue repair once the infection is under control
complement protiens
activated in a cascade, group of 25 plasma proteins and cel membrane proteins
intermediates of the complement cascade
- act as opsonins C3b
- act as leukocyte attractants C39
- induce mast cell degranulation C39/5a
- form membrane attack complex to lyse the target cells
bradykinin
RPPGFSPFR
generated through proteolytic cleavage of plasma protein kininogen
causes vasodilation, lower BP, increased vascular permeability, promotes pain sensation (hyperalgesia)
acute-phase proteins
plasma level increases immediately after injury or infection and declines as the immune response proceeds, mostly produced by the liver, includes opsosins, antiprotease molecules, C-reactive protien
antiprotease
in acute-phase protiens, prevent tissue damage
CPR
binds to lysophospho choline on the surface of dead or dying cells and some bacteria and activates the complement system promoting phagocytosis by macrophages- indicator of chronic inflammation (level correlates with risk for CHD)
histamine
one of initiators of inflammatory response - synthesized and stored in the granules of basophils, mast cells and released upon degranulation
histamine functions
- Dilates blood vessels and increases blood flow. (redness)
- Increases capillary permeability, plasma proteins escape
into the interstitial space, leading to local edema.
(swelling, nasal congestion) - Works with prostaglandins and leukotrienes to induce
bronchoconstriction. (asthma, anaphylactic shock)
eicosanoids
Cytokines and complement stimulate the enzymatic release
of arachidonic acid from plasma membrane (glucocorticoids).
cyclooxygenase pathway
COX‐2 is induced by LPS, TNFD and IL‐1, and inhibited by
glucocorticoids. PGE2s cause vasodilation, hyperalgesia,
fever. ..
lypogenase pathway
leukotrienes cause bronchoconstriction (asthma)
Lypoxins modulate the actions of leukotrienes and
cytokines (resolution of inflammation).
acute inflammatory response cytokines
tumor necrosis factor‐alpha (TNFalpha) are two major
cytokines involved in acute inflammatory response.
1) stimulate hepatic production of acute‐phase proteins; 2)
alter vascular endothelium to facilitate passage of leukocytes
and proteins; 3) induce fever; 4) stimulate cytokine secretion.
TNF alpha
produced chiefly by activated macrophages: 1) stimulate
hepatic production of acute‐phase proteins; 2) neutrophil
chemoattractant; 3) pyrogenic; 4) induce apoptosis.
phagocytic Cell defect- chronic granulomatous disease
cause: phagocyte NADPH oxidase
consequence: bacterial/fungal infections (pneumonia, bacteremia), granuloma formation
treatment: antibacterial and anti-fungal agents, IFN-gamma, bone marrow transplantation
leukocyte Adhesion Deficiency (LAD) cause
LAD1 defective IFA-1 - ineffective migration and phagocytosis
leukocyte Adhesion Deficiency (LAD) consequences
recurrent bacterial infections, inefficient wound healing, impaired pus formation, high granulocyte level in peripheral blood (granulocytes or neutrophilia), granulocytosis (increased level of granulocytes in the peripheral blood)
leukocyte Adhesion Deficiency (LAD) treatment
early antimicrobial therapy, hemopoietic stem cell transplant
C3 deficiency
C3 is common to all pathways of complement activation. recurrent and often severe bacterial infections
lectin pathway deficiency
recurrent bacterial infections in early childhood, before establishing Ig repertoire
deficiency in early components of the classic pathway
immune complex diseases and autoimmune disease such as SLE and glomerulonephritis
deficiency in late-acting complement components
impaired MAC formation (Neisseria infection) but competent in opsonization and inflammation initiation`
treatment of complement system deficiency
antimicrobial therapy (antibiotics), purified complement components (but has short half life)
X-linked agammaglobulinemia (XLA) cause
mutations in the bruton tyrosine kinase gene, involved BCR signaling
X-linked agammaglobulinemia (XLA) consequences
lack of mature B cell and plasma cells, lack all Ig classes, recurrent infections starting 5-6 months of age
X-linked agammaglobulinemia (XLA) treatment
antimicrobial therapy, intravenous immunoglobulins containing high IgG levels
selective IgA deficiency cause
reduced level of IgA but normal levels of other isotypes, genetic cause is unclear
selective IgA deficiency consequences
asymptomatic or slightly increased frequency of respiratory tract infections
selective IgA deficiency treatment
treatment of associated infections, no specific immunotherapy required
X-linked hyper IgM (XHIM) syndrome cause
T helper cells lack CD40 ligand important for isotype switching and memory B cell generation
X-linked hyper IgM (XHIM) syndrome consequences
high levels of serum IgM and very low levels of serum IgG, IgA, IgE, recurrent bacterial infections, recurrent neutropenia and anemia
X-linked hyper IgM (XHIM) syndrome treatment
antimicrobial therapy, intravenous immunoglobulins (IVIG), bone marrow transplantation
DiGeorge Syndrome (congenital thymic aplasia) cause
failure of the thymus to develop normally during embryogenesis (so you can’t produce t-cells)
DiGeorge Syndrome (congenital thymic aplasia) pathological consequences
- undetectable cell-mediated immune response
- recurrent or chronic infections with virus, bacteria, fungi, protozoa
- cardiac, renal and eye anomalies, hypoparathyroidism and skeletal defects
DiGeorge Syndrome (congenital thymic aplasia) treatment
partial hypoplasia: recovers thymus function
postnatal transplantation of cultured thymus tissue
severe combined immunodeficiency (SCID) cause
defects in cytokine receptors or kinase, TCR complex, recombinases in gene rearrangement of TCR and BCR and MHC-II expression
severe combined immunodeficiency (SCID) consequence
loss of B and T cell systems
severe, recurrent infections commencing the first few months of life
will not survive the first year of life
severe combined immunodeficiency (SCID) treatment
immune system reconstitution by hematopoietic stem cel transplantation
secondary immunodeficiencies
malnutrition, lymphoproliferative disease, AIDS, microorganisms
malnutrition
cell proliferation and protein synthesis
lymphoproliferative disease
leukemia, myeloma, hypogammaglobulinemia, defective cell-mediated immune function sometimes
secondary immunodeficiencies medical treatment
radiation, chemotherapy, corticosteroids, immunosuppressants
secondary immunodeficiencies microorganisms
suppress the immune response (e.g. cytomegalovirus, measles, rubella, epsein-barr virus)
AIDS
HIV selectivity infects CD4 T cells leading to gradual depletion of helper T cells
hypersensitivity
damaging inflammatory immune response to a nonpathogenic antigen (allergen) or an exaggerated response to a pathogen
first response to allergen
- allergen ingested and processed by antigen presenting cell
- this cell activates helper t cells
- activated helper t cells activate b lymphocytes
- b lymphocytes become plasma cells and memory cells
- b and t cells retain memory of exposure to the antigen
reexposure to the allergen
upon reexposure to the allergen, B and T cells activate more quickly. the body reacts strongly with the release of histamine, cytokines, and other mediators causing an allergic reaction
allergens
induce type I and IV hypersensitivity, almost always low molecular-weight proteins; many attach to airborne particles
allergy genetic factors
association between atopy (heightened immune response) and specific HLA (human leukocyte antigen) loci, and polymorphisms of several genes encoding the high affinity IgE receptor, IL-4 receptor, IL-4 and IL-13
allergy environmental factors
interact with genetic factors to maintain TH2 (antibody mediate immunity) cell-directed immune response which activates eosinophils and promotes IgE production
allergy early childhood exposure
to bacterial and viral infections and endotoxins (LPS) helps shift native TH2-cell response to TH-1 cell response , reducing the tendency to allergy
allergy pollutants
small chemicals in body bind to proteins to display immunogenicity
type I hypersensitivity
immediate, IgE decorated mast cells or basophils degranulate within minutes of binding, anaphylatoxins (C3, C5) can cause IgE mast cell degranulation, so do some food additives and drugs (asprin) - the hapten binds to the protein which then binds to the mast cell and without IgG causes degranulation
histamine (H1R)
type I mediator
smooth muscle: airway constriction, systemic vasodilation, gastric muscle contraction
endothelium: increased vascular permeability
sensory nerves: itching and urticaria (hives)
CNS: circadian cycle modulation (drowsiness)
prostaglandins and leukotrienes
type I mediator
prolonged bronchoconstriction and continued vascular permeability
cytokines
type I mediator, leukocyte differentiation and recruitment
anaphylatoxins
type I mediator, (C3a and C5a): IgE independent mast cell degranulation
atopy
exaggerated IgE-mediated immune response and hype I. atopic indivuals have a greater tendency to develop IgE mediated responses (genetics)
type I clinical conditions
allergic rhinitis, conjuctivis, allergic asthma, food allergies, anaphylaxis, atopy
anaphylaxis
(without guarding) a sudden, systemic atopy characterized by shock (low blood pressure and loss of fluid), bronchospasm, and cardiovascular collapse- caused by bee and wasp stings, food, penicillin
type I clinical test
skin prick an antigen specific serum IgE
type I treatment
avoid exposure, epinephrine (airway in anaphylaxis, Epipen), antihistamines (benadryl), corticosteroids, anti-IgE monoclonal antibody, mast cell stabilizer, desensitation (food)
how to make benedryl non-sedating
put a charge on it to prevent the drug from crossing into the CNS
H2R antagonists
Gi- mucus and antiacid secretions
mast cell stabilizer
sodium cromoglycate
type II
antibody dependent cellular toxicity
type II trigger
foreign antigen absorbed to cell membrane or extracellular matrix- leads to antibody mediated cell damage
type II immunoglobulins
IgM and IgG- activate complements
NO IgE
type II immune cells
NK cells, eosinphils, neutrophils, macrophages (help phagocytote)
type II mediators
complement
type II pathophysiology
ADCC (antibody dependent), complement-dependent cytotoxyicty (CDC), opsonization, phagocytosis causing tissue damage (hemolysis), hemolytic anemia
ADCC
IgG binds to antigens, causes the NK cell to bind, causes lyses, antibody bound to cell-surface epitopes, epitope binding causes conformational change in Fc - leads to cell lysis (no RBC/nucleated cell)
CDC
antibody binds to the epitopes and triggers the complement system, loss of electrolytes because pokes a hole to cause lyses and secretion of inflammatory mediators - antiglomerular basement membrane (good pastures syndrome)
hemolytic anemia
IgM anti-group A causes phagocytosis, complement mediated lysis,
ex: blood donor A given to blood donor B,
related disorders to type II hypersenstitivity
ABO transfusion reactions, hemolytic disease of newborn (Rh-negative mother with Rh-positive child), type II reactions (penicillin, cephalosporins, quinidine cause hemolytic anemia) sensation phase 7-10 days and secondary response is < 3 days
anti-glomerular basement membrane disease (good pastures), hyper acute graft rejection of organ transplant (attack of antibody and complement)
type III hypersensitivity
immune complex (antibody + antigen) disease, circulating immune complexes (mostly IgG and IgM) deposit in vasculature or tissue (joint, glomeruli) causing damage via complement, phagocytes and inflamatory mediators
type III pathophysiology
- Fc receptors on the endothelium bind antitoxin (antibody that has reacted with toxoid)
- additional antitoxin and toxoid bind to form larger complexes
- the classical pathway of complement activated. anaphylotoxins, C5a, C4a, C3a are released attracting macrophages and neutrophils
arthrus reactions symptoms
localized cutaneous inflammatory reactions due to immune complexes, inflammation in dermal blood vessels following injection of large amounts of antigens
cause of arthus reactions
drug injections (b-lactam-based antibiotics, heparin, fetal calf serum) into sensitized individual, vaccines, insect stings and spider bites
characteristics of arthus reactions
edematous (swelling) and erythematous reaction (rash) after 3-8 hours of exposure
arthus reaction pathophys
- locally injected antigen in immune individual with IgG antibody
- local immune complex formation
- activation of FcgammaRIII on mast cells induce degranulaiton
- local inflammation, increased fluid and protein release, phagocytosis, and blood vessel occlusion
serum sickness
systemic immune complex reaction after injection of a large quantity of foreign materials, deposit in small blood vessels, complement dependent inflammation, vasculititis, fever, joint pain, hives, splenomegaly, heterologous antiserum, antitoxin, IVIG and IV drugs, 7-10 days primary response 2-4 days secondary response. complections rare, treatment symptomatic
inhalation of antigenic particles
farmers lung, apergillus (fungi) spores IgE and IgG generation and TH1 activation, proinflammatory cytokines and tissue damage
inhalation of antigenic particles symptoms
asthma with fever, cough, chronic lung damage (permanent radiological damage to the lungs)
other related type III disorders
SLE (systematic lupus erythematosis) RA, leukocytolastic vasculitis, cryoglobemia (antibody out of solution), acute hypersensitivity pneumonitis, certain glomerulonephritis
type IV hypersensitivity
delayed or cell-mediated, triggered by antigen fragment in complex with MHC-II on APC, mediators TH1, TH2, Tc cells, cytokines, macrophages, leads to tissue damage,
Type IV symptoms
takes several days to develop, cytokine storm, causes macular rashes, fever, hypotension, organ failure
Contact dermititis common allergens
metal, plastic, rubber, latex, plant chemicals, medications (neomycin and phenothiazines) urushiol is the hapten responsible for contact dermatitis with poison ivy
contact dermititis symptoms
red rash, bumps, weeping blisters, swelling and intense itching
contact dermatitis treatment
topic steroids (triamcinolone, clobestasol), systematic corticosteroid therapy when severe cases
contact dermatitis pathophys
chemically active compound (hapten) applied to skin, CD4+T cells enter site, recognize hapten-protein conjugate release bioactive molecules, macrophages and other phagaocytse enter site to cause inflammation
TB skin test (mantoux skin test)
injection of purified protein derivative (PPD) into the skin of individual previously infected with mycobacterium TB, recruits and activates specific immune cells and present with redness and palpable induration at 48 to 72 hours
non-topical delayed-type hypersensitivity
sub q intro of foreign substance, dendritic cells and macrophages release chemo-attractants, CD4+T cells enter site and recognize foreign substance and release bioactive molecules, macrophages and other phagocytes enter site to cause inflammation
T-cell mediated cytotoxicitiy
chemically bound active coupmound (hapten) applied to skin, hapten binds to pMHC class I on cell surface, cells release chemical signals, CD8+ Tcells enter the site, CD8+ T cells (cytotoxic T lympocytes) destroy hapten conjugated cells and release mediators and phagocytes enter
celiac disease
autoimmune disorder, allergen gluten
TH and TC cells infiltrate in the gut epithelial membrane and lamina propria, expression of pro-inflammatory cytokines and production of IgA and IgG antibodies directed against gluten as well as host components. inflammation, villous atrophy and crypt hyperplasia in small intestine, bone disease, anemia, endocrine disorders, neurological effects- need gluten free diet - not strictly type 4
