Chapter 3 Flashcards
types of T lymphocytes
Helper T cells, cytotoxic T cells, suppressor T cells
how many binding sites does the T cell receptor have
1
antigen presentation
required for T cells
APC
antigen presenting cells
types of APC
macrophages
dendritic cells
B cells
what is the best type of APC
dendritic cell
major histocompatibility proteins (MHC)
present antigen to responding cells of immune system (T cells)
MHC Class I
present on all cells w/nucleus
CD8+
what are MHC I not present on
red blood cells
MHC Class II
only on APCs
CD4+
sequence of humoral immunity (B lymphocyte)
- B cell sees virus (must interact w/helper T cell)
- B cell becomes plasma cell
- Memory B cells are formed
sequence of cellular immunity (T lymphocyte)
- Cytotoxic T cells kill epithelial cells attacked by virus (helper T cells assist)
- Memory cells are left over
types of immune response
primary and secondary
primary immune response
first exposure
naive cells
secondary immune response
follows initial encounter’s formation of memory cells
AKA activating memory cells
basis of vaccines
what immunoglobulin is made first
IgM
hypersensitivity
too much of a response to the wrong antigen
immunodeficiency
too little of a response to antigen
autoimmune disease
inappropriate response to antigen
malignancy
cancer of immune tissues
types of hypersensitivity reactions
type 1, 2, 3, 4
what types of hypersensitivity reactions are mediated by B cells and antibodies
types 1, 2, 3
what type of hypersensitivity reaction is mediated by T cells
type 4
time frame of Type 1 hypersensitivity
immediate/instantly
what kind of antibodies are involved in hypersensitivity
preformed antibodies (already encountered antigen)
IgE antibody is made after first exposure
what does the IgE antibody do in Type 1 hypersensitivity
becomes embedded in mast cell, binds, degranulates
what cells are involved in Type 1
mast cells and basophils
mast cells in Type 1
affect smooth muscle because they are full of granules, also mediated by prostaglandins (derivatives of arachidonic acid)
effect of granules in mast cells (Type 1)
degranulation (histamine and serotonin)
vasodilation, increased capillary permeability, edema accumulation BLOOD VESSELS
is Type 1 hypersensitivity systemic or local?
both
systemic Type 1 hypersensitivity effects
enters blood, activating massive amounts of mast cells, leading to constriction, decreasing BP
local Type 1 hypersensitivity effects
nose, sinuses, GI tract
phase of IgE-mediated allergic reaction (Type 1)
immediate (wheel & flare)
late (eosinophil chemotaxis)
what is the main ‘disease’ of Type 1 hypersensitivity
allergic
hypersensitivity to environmental substance
atopy
genetic sensitivity
what is the most common allergen?
dust mites
examples of Type 1 hypersensitivity
hay fever, hives, atopic dermatitis (eczema), systemic anaphylaxis, asthma
why are mast cells important for parasitic infections
IgE ejects parasites
helminth
parasitic
hygiene hypothesis
westernized countries have allergic disorders vs. developing countries do not
treatment for Type 1 hypersensitivity
avoidance, drugs
anti-histamines, corticosteroids, anti-IgE therapy, beta adrenergics, desenstitization
anti-histamine
blocks vasoactive histamine receptors
corticosteroids
decreases immune system by decreasing cortisol levels
anti-IgE therapy
IgE to IgG antibodies
beta adrenergics
albuterol, opens airways by SNS
what is Type 2 hypersensitivity
cytotoxic (attacks host cell)
tissue specific antibody attaches directly to antigen in target tissue
what cells mediate Type 2
B cells
what antibodies are included in Type 2
IgG or IgM
types of interaction in Type 2
death of target cells
antibodies block receptor function (myasthenia gravis)
examples of Type 2 hypersensitivity
transfusion reactions, hemolytic disease of newborn (Rh factor), autoimmune reaction (myasthenia gravis)
what is Type 3 hypersensitivity
normal immune complex
what is Type 3 mediated by
antibody and antigen (forms immune complex)
what is Type 3 cleared by
red blood cells
main point of Type 3
failure to clear complexes
- deposition induced inflammatory response in blood vessels, kidneys, joints
is Type 3 deposition local or systemic?
can be distant (systemic)
circulates via blood to different site from formation
can also be local
remains at site (farmer’s lung)
what is Type 3 influenced by
size of complex (smaller complexes circulate longer, increasing immune response)
vascular permeability
what is a good word to describe Type 4 hypersensitivity
delayed
does Type 4 depend on antibodies?
no
what mediates Type 4
T lymphocytes
steps of Type 4 hypersensitivity
- initial sensitization via antigen uptake, hapten, presentation by APC
- APCs present to Helper T cells
- memory T cells migrate to site
- second exposure releases mediators, attracting other cells
hapten
part of antigen binding to normal protein
examples of Type 4 hypersensitivity
poison ivy, metallic injury, tuberculosis test
what is an autoimmune disease
attacks self, self becomes foreign
examples of autoimmune diseases
SLE, RA, myasthenia gravis, Type I Diabetes, MS
why does the body turn on itself?
imperfect B/T cell programming
inaccessible self-antigens
altered antigen
molecular mimicry
infection and inflammation (viral)
decrease suppressor T cell function
genetic susceptibility (MHC proteins)
molecular mimicry
Type 2 hypersensitivity
foreign antigen resembles pathogen and host antigen, immune response initiated by microbe becoming directed at self cells
what is the most common autoimmune disease
type 1 diabetes
examples of molecular mimicry
rheumatic fever
Systemic Lupus Erythematosus (SLE)
Lupus
systemic autoimmune disease
hallmarks of lupus
butterfly rash
women (20-40yrs)
fever
weakness
photosensitivity
arthritis and kidney dysfunction can develop
is lupus age associated?
no
what type of hypersensitivity is lupus
Type 3 hypersensitivity
what antibodies are associated with lupus
antinuclear antibodies (ANA) in blood
highly sensitive, low specificity
what do ANA do in lupus
binding of ANA forms soluble immune complexes, leading to deposition
what does the deposition of immune complexes cause in lupus
inflammation (in the arteries, results in vasculitis)
is lupus a chronic inflammatory disease?
yes. it affects all tissues of body KIDNEYS
clinical findings of lupus
cytopenia
vasculitis
skin lesions
myocarditis
glomerunephritis
arthritis
brain (microinfarcts, psychosis, dementia)
cytopenia
decrease in # of WBC
vasculitis
inflammation of blood vessels, weakens and causes redness of skin
myocarditis
inflammation of heart muscle
microinfarcts
decrease in blood flow, leads to cell death
how do you diagnose lupus
blood work
look for presence of ANA
high ESR and CRP levels
clinical outcome of lupus
variable and unpredictable,
30% mortality rate in first 10 yrs (reduced life expectancy)
death due to organ failure (kidneys, brain)
treatment for lupus
mild=NSAIDs
severe= corticosteroids, antineoplastic
what do NSAIDs do
decrease inflammation
antineoplastic
cancer treatment drugs, decrease cell division to reduce # of WBC
drug induced lupus
following exposure to drugs, lupus-like symptoms form
~10% of cases
rheumatoid arthritis
systemic autoimmune disease
1-3% of population
episodic
what type of hypersensitivity is rheumatoid arthritis
Type 3
group most susceptible to RA
women, 20-40yrs
is RA age-associated
no
episodic
relapse to remission to relapse to remission
what organs/tissues does rheumatoid arthritis affect
lungs, bone, cartilage, pericardium
rheumatoid factor
autoimmune antibodies
progression of RA
starts in small joints of hands and feet, synovial membrane is attacked with T cell deposition
Sjogren syndrome
autoimmune disease of lacrimal and salivary glands
characteristics of Sjogren syndrome
dry irritated red eyes, dry mouth, difficulty swallowing, extraglandular (vasculitis, neuropathy, lymphoma)
neuropathy
nerve destruction
lymphoma
cancer of lymphocytes
Sjogren syndrome treatment
eye drops, drinking fluids
amyloidosis
amyloid proteins are abnormally deposited on organs and interfere w/function
types of amyloidosis
primary
secondary
primary amyloidosis
no known cause
antibodies form amyloid light chain which breaks down
secondary amyloidosis
secondary to some other condition (SLE, RA)
amyloidosis treatment
replace bone marrow
symptoms of amyloidosis
depends on tissue/organ of deposits
types of transplantation
autograft
homograft
allograft
xenograft
autograft
own skin
homograft
genetically identical twin
allograft
genetically different but same species
xenograft
different species
pig valve
what is transplantation rejection mediated by
immune system
what causes transplantation rejection
mismatch of MHC
what causes transplantation rejection
mismatch of MHC
types of transplantation rejection
hyperacute organ rejection, acute organ rejection, chronic transplant rejection
hyperacute organ rejection
preformed antibodies react w/graft endothelial cells
INSTANT
what causes hyperacute organ rejection
previous organ transplant, blood transfusion, pregnancy
acute organ rejection
happens within weeks of transplant, attach to mismatch of MHC
what mediates acute organ rejection
T cells
chronic transplant rejection
months to years post transplant
T cell mediated
what happens w/chronic transplant rejection
ischemia and hypoperfusion of organ
graft vs. host reaction (GVH)
bone marrow transplants
recipients must have pretransplant treatment (killing off bone marrow for space)
mechanisms of GVH
immune cells in graft recognize host as foreign
transplanted graft lymphocytes attack host cells
what tissues are affected by GVH
GI tract (diarrhea)
skin (red/rash)
liver (jaundice)
how do you minimize GVH
matching MHC proteins prior to transplant
blood transfusion
most common form of transplantation
blood type for matching of donors and recipients
transfusion reaction
antibodies mismatch
ABO
antigens on surface of RBC
Type A
A antigen makes B antibodies
can receive A, O
Type B
B antigen makes A antibodies
B, O
Type AB
no antibodies to A or B
UNIVERSAL RECIPIENT A, B, AB, O
Type O
no antibodies on surface but makes antibodies to A and B
UNIVERSAL DONOR O
major transfusion reaction
hemolysis, thrombosis
life threatening
hemolysis
RBC destruction
thrombosis
abnormal blood clot due to stickiness
minor transfusion reaction
fever, chills
not life threatening
not due to ABO mismatch (due to other antibodies)
Rh incompatability
D/d antigens
hemolytic disease of newborn (Rh+)
crossmatch
donor blood is compatible w/recipient blood
major crossmatch
donor’s RBC in recipient’s serum
checks for preformed antibodies in recipient’s serum against donor’s RBC
minor crossmatch
donor’s serum in recipient’s RBCs
preformed antibodies in donor serum that could hemolyse recipient’s RBC
types of immunodeficiency diseases
primary (born w/it) or secondary (acquired)
deficiency of T cells
prone to infections, cancer (T cells kill cancer cells)
SCID (severe combined immunodeficiency diseases)
immunodeficiency diseases
entire immune system or subsets of cells are effected
deficiency of B cells
lack of antibodies
sensitive to bacteria
X-linked Agammaglobulinemia (XLA)
primary immunodeficiency disease
what does XLA lack
antibodies, tyrosine kinase which leads to B cell development
is XLA an SCID
no
what results from XLA
recurrent bacterial infections (no B cells, no antibodies)
DiGeorge Syndrome
deletion of Q arm on chromosome 22 (primary immunodeficiency disease)
is DiGeorge Syndrome an SCID
yes
what happens with DiGeorge Syndrome
missing genes, no thymus development, no T cells
causes of secondary immunodeficiency diseases
secondary to something else:
nutrition, infection, radiation, age
AIDS
secondary immunodeficiency disease
caused by HIV
characteristics of AIDS
low Helper T cell count
recurrent infections (opportunistic infections)
neoplasms
cachexia
cachexia
wastes away
transmission of AIDS
blood and bodily fluids (semen, blood transfusions, mom to baby)
highest risk groups for AIDS
homosexual or bisexual males
IV drug users
patients w/hemophilia (missing coagulation factors)
blood transfusion recipients
heterosexual contacts w/those above
HIV
secondary immunodeficiency disease
virus (nucleic acid in protein coat)
how does HIV enter cells
binding to receptors through retrovirus of RNA and DNA
what does HIV entry depend on
CD4 receptor AND CCR5 (or CXCR4) co-receptor
progression of HIV
acute, latent, crisis
opportunistic infections of AIDS
candidasis, tuberculosis, salmonella, herpes
neoplasms of AIDS
kaposi sarcoma, lymphoma brain
neurological symptoms of AIDS
dementia, seizures, mood swings
HIV resistant mutation
CCR5 mutation
virus can’t get into cell
heterozygous
in latent period for longer, cell can still enter
homozygous
virus doesn’t progress at all
ethnicity of HIV
white
10% hetero 1% white
HIV/AIDS diagnosis
anti-HIV antibodies, HIV antigens in blood and saliva
clinical diagnosis of AIDS
definitive w/out confirming lab data (kaposis sarcoma < 60yrs)
definitive w/confirming data (CD4+ <200 cells/mL)
presumptive w/conforming lab data (recurrent pneumonia)
goals of HIV treatment
control virus and other infections
HIV treatment
highly active antiretroviral therapy (HAART)
HAART
suppresses virus replication, acts on different stages of HIV life cycle, increases latency period
