Immuno USMLE Flashcards
a secondary lymphoid organ that has many afferents & 1 or more efferents. It is encapsulated, with trabeculae.
lymph node
fxs of lymph node (3)
1) filtration by macrophages
2) storage/proliferation of B and T cells
3) antibody production
this part of the lymph node is the site of B-cell localization and proliferation.
follicle
these follicules have pale central germinal centers and are active.
secondary follicles
this part of the lymph nodes consists of closely packed lymphocytes and plasma cells and sinuses that communicate with efferent lymphatic and contain reticular cells and macrophages
medulla
this part of the lymph node houses T cells. It is the region of the cortex between follicles and medulla. It contains high endothelial venules through which T and B cells enter from the blood. In extreme cellular immune response (i.e., viral) the this becomes greatly enlarged.
paracortex
paracortex is not well developed in pts with this syndrome
DiGeorge syndrome
this duct drains the right arm and right half of the head
right lymphatic duct
this duct drains the right arm and right half of the head
right lymphatic duct
this duct drains everything besides the right arm and right half of the head
thoracic duct
these are long vascular channels in red pulp with fenestrated “barrel hoop” basement membrane. Macrophages are found nearby.
sinusoids of the spleen
these cells are found in the periarterial lymphatic sheath (PALS) and in the red pulp of the pleen.
T cells
these cells are found in the follicles within the white pulp of the spleen
B cells
this is the site of T-cell maturation.
thymus
mneu: think of the Thymus as “finishing school” for T cells. They arrive immature and “dense” in the cortex; they are mature in the medulla.
the thymus is from the epithelium of this branchial pouch.
3rd
In the thymus, the cortex is dense with this type of T cells; while the medulla is pale with this type of T cells and epithelial reticular cells and Hassall’s corpuscles.
immature
mature
In the corticomedulary junction only T cells with MHC restriction are chosen, this is called?
then only T cells that are non-reactive to self are chosen.
what is this called
positive selection
negative selecton
this type of T cell produces IL-2 & gamma interfereon in order to activate macrophages and Tc cells
Th1 cells
this type of T cell produces IL-4 & IL-5 to help B cells make Ab
Th2 cells
B=2nd letter of the alphabet
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Host defense against infection (opsinize bacteria, neutralize toxins & viruses)
Ab mediated immunity (B cells)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Host defense against Mycobacterium tuberculosis, virus infected cells, and fungi.
Cell mediated immunity (T cells)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Host defense against Mycobacterium tuberculosis, virus infected cells, and fungi.
Cell mediated immunity (T cells)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Allergy (e.g., hay fever, type I hypersensitivity)
B (Ab mediated immunity)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells: Allergy to poison oak, type IV hypersensitivity
Cell-mediated immunity (T cells)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Autoimmunity
B cell (Ab mediated immunity)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Graft & tumor rejection
T cell(Cell mediated immunity)
State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
help and supression of Ab response
T cell(Cell mediated immunity)
MHC stands for
major histocompatibility complex
give the 3 class I genes
A,B,C
give the 3 class I genes
A,B,C
give the 3 MHC class II genes
DP,DQ,DR
this type of MHC has 1 polypeptide, with B2-microglobin
Class I
this type of MHC has 2 polypeptides, with an alpha and a beta chain
class II
this type of cells have MHC II & MHC I proteins
APCs (e.g., macrophages & dendritic cells)
This class of MHC are the main determinants of organ rejection
class II
this type of Ag loading occurs in RER (viral Ag)
MHC I
this type of Ag loading occurs in acidified endosome
MHC II
Give the 2 T-cell glycoproteins
CD4
CD8
helper T cells have CD_, which binds to MHC II on APCs
4
mneu: product of CD & MHC =8
Cytotoxic T cells have CD__, which binds to MHC I on virus infected cells
8
mneu: product of CD & MHC =8
this is a cluster of polypeptides associated with a T-cell receptor. It is important in signal transduction
CD3 complex
give the 3 Ag presenting cells
1) macrophage
2) B cell
3) dendritic cells
in this type of T cell activation:
1) foreign body is phagocytosed by APC
2) Foreign Ag is presented on MHC II and recognized by TCR on Th cell
3) “Costimulatory signal” is given by interaction of B7 & CD28
4) Th cell is activated to produce IL-2 and gamma-interferon
Th activation
In this type of T cell activation:
1) Endogenously synthesized (viral or self) proteins are presented on MHC I and recognized by TCR on Tc cell
2) IL-2 from Th cell activates killing of the virus infected cell.
Tc activation
_______ part of L & H chains recognize Ag.
variable
_______ part of H chain of IgM & IgG fixes complement
Constant
_______ chain contributes to Fc and Fab fractions
Heavy
_____ chain contributes only to Fab fraction
light
This fragment of Ab is constant, has a carboxy terminal, is complement-binding (IgG & IgM only) and has carbohydrate side chains
Fc fragment
Abs do many things to aid in host defense. This method of host defense refers to when Ab promotes phagocytosis. image. p.184
opsonization
Abs do many things to aid in host defense. This method of host defense refers to when Ab prevents bacterial adherance. image. p.184
neutralization
Abs do many things to aid in host defense. This method of host defense refers to when Ab activates compliment, enhancing opsinization and lysis. image. p.184
complement activation
Ab diversity is generated by:
1) random ______ of VJ (light chain or VDJ (heavy chain) genes)
2) random ______ of heavy chains with light chains
3) Somatic __________
4) addition of DNA during _________ by terminal deoxynucleotidl transferase
recombination
combination
hypermutation
genetic recombination
mature B lymphocytes express ______ & _____ on their surfaces.
IgM & IgD
mature B lymphocytes express IgM & IgD on their surfaces may differentiate by isotype switching (mediated by cytokines and CD40 ligand) into plasma cells that secrete ____,____ or _____
IgA, IgE, or IgG
this immunoglobin isotype is the main Ab in secondary response. It is the most abundant. It fixes complement, crosses the placenta, opsonizes bactera, & neutralizes bacterial toxins & viruses
IgG
This immunoglobin isotype prevents attachment of bacteria and viruses to mucous membranes, it does not fix complement. It can be a monomer or dimer. It is found on secretions. It picks up secretory component from epithelial cells before secretion.
IgA
this immunoglobin isotype is produces in the primary response to an antigen. It fixes complement but does not cross the placenta. The Ag receptor is on the surface of the B cells. It can be a monomer or pentamer.
IgM
this immunoglobin isotype is found on the surface of many B cells and in serum. Its fx is unclear.
IgD
this immunoglobin isotype mediates immediate (type I) hypersensitivity by inducing the release of mediators from mast cells and basophils when exposed to allergen. It mediates immunity to worms. It is the lowest Ig isotype in serum
IgE
This is an Ig epitope that differs among members of the same species. It can be on light or heavy chain
allotype (polymorphism)
This Ig epitope is common to a single class of Ig (5 classes determined by the heavy chain)
Isotype (IgG, IgA, etc.)
Isotype=iso (same) common to same class)
This Ig epitope is determined by the Ag binding site
Idiotype (specific for a given Ag)
Idiotype=idio (unique)
hypervariable region is unique
This important cytokine is secreted by macrophages. It stimulates T cells, B cells, neutrophils, fibroblasts, and epithelial cells to grow, differentate, or synthesize specific products. It is an endogenous pyrogen
IL-1
mneu: HOT T-BONE stEAk IL-1: fever (HOT) IL-2: stimulates T cells (T) IL-3: stimulates BONE marrow IL-4: stimulates IgE (E) IL-5: stimulates IgA (A)
This important cytokine is secreted by Th cells. It stimulates growth of helper and cytotoxic T cells
IL-2
mneu: HOT T-BONE stEAk IL-1: fever (HOT) IL-2: stimulates T cells (T) IL-3: stimulates BONE marrow IL-4: stimulates IgE (E) IL-5: stimulates IgA (A)
This important cytokine is secreted by activated T cells. It supports the groth and differentiation of bone marrow stem cells. It has a fx similar to GM-CSF
IL-3
mneu: HOT T-BONE stEAk IL-1: fever (HOT) IL-2: stimulates T cells (T) IL-3: stimulates BONE marrow IL-4: stimulates IgE (E) IL-5: stimulates IgA (A)
This important cytokine is secreted by Th cells. It promotes groth of B cells. It enhances class switching of IgE & IgG
IL-4
mneu: HOT T-BONE stEAk IL-1: fever (HOT) IL-2: stimulates T cells (T) IL-3: stimulates BONE marrow IL-4: stimulates IgE (E) IL-5: stimulates IgA (A)
This important cytokine is secreted by Th cells. It promotes differentiation of B cells. It enhances class switching of IgA. It stimulates production and activation of eosinophils
IL-5
mneu: HOT T-BONE stEAk IL-1: fever (HOT) IL-2: stimulates T cells (T) IL-3: stimulates BONE marrow IL-4: stimulates IgE (E) IL-5: stimulates IgA (A)
This important cytokine is secreted by Th cells and macrophages. It stimulates production of acute phase reactants and immunoglobins.
IL-6
This important cytokine is a major chemotactic factor for neutrophils
IL-8
This important cytokine is secreted by B cells and macrophages. It activates NK and Th2 cells
IL-12
This important cytokine is secreted by Th cells. It stimulates macrophages
gamma interferon
This important cytokine is secreted by macrophages. It increases IL-2 receptor synthesis by Th cells. It increases B cell proliferation. It attracts and activates neutrophils. It stimulates dendritic cell migration to lymph nodes.
TNF-alpha
given the cell surface proteins give the cell:
CD4,TCR,CD3,CD28,CD40L
helper T cells
given the cell surface proteins give the cell:
CD8,TCR,CD3
cytotoxic T cells
given the cell surface proteins give the cell:
IgM,B7,CD19,CD20,CD40, MHC II
B cells
given the cell surface proteins give the cell:
MHC II,CD14, receptors for Fc & C3b
Macrophages
given the cell surface proteins give the cell: Receptors for MHC I, CD16
NK cells
MHC I
all cells except mature red cells
This system is a system of proteins that interact to play a role in humoral immunity and inflammation
compliment
complement defends against this type of bacteria
G-
compliment is activated by Ig_ & Ig_ in the ______ pathway,
and activated by molecules on the surface ofmicrobes (especially endotoxin) in the ________ pathway
G & M, classic
alternate
mneu: GM makes CLASSIC cars
given the complements give the function:
C1,C2,C3,C4
viral neutralization
given the complements give the function:
C3b
opsonization
given the complements give the function:
C3a,C5a
anaphylaxis
given the complements give the function:
C5a
neutrophil chemotaxis
given the complements give the function:
C5b-9
cytolysis by membrane attack complex (MAC)
deficiency of _______ leads to hereditary angioedema (overactive complement)
C1 esterase inhibitor
deficiency of _______ leads to severe, recurrent pyogenic sinus and respiratory tract infections
C3
deficiency of _______ leads to Neisseria bacteremia
C6-C8
deficiency of _______ leads to leads to paroxysmal nocturnal hemoglobinuria (PNH)
DAF
these are proteins taht place uninfected cells in an antiviral state
interferons (alpha, beta,gamma)
Interferons induce the production of a 2nd protein that inhibits viral ______ by degrading viral mRNA (but not host mRNA)
protein synthesis
alpha and beta interferons inhibit viral ________
protein sythesis
gamma interferons increase ________ expresssion and antigen presintation in all cells
MHC I & II
interferons activate these cells to kill virus-infected cells
NK cells
this type of immunity is induced after exposure to foreign Ag. It has a slow onset and provides long lasting protection (memory)
active immunity
this type of immunity is based on recieving preformed Ab from another host. There is a rapid onset but a short life span of the Ab
passive immunity
what are some common exposures in which pts are given preformed Abs (passive immunity)
Tetanus Toxin
Botulism Toxin
HBV
Rabies
mneu: To Be Healed Rapidly
Classic examples of antigen variation include this bacteria with 2 flagellar varients
salmonella
Classic examples of antigen variation include this virus that undergoes antigen shift and antigen drift
influenza
Classic examples of antigen variation include this parasite that undergoes programmed rearrangement
trypanosomes
Some mechanisms for Ag variation include DNA rearrangement and RNA segment rearrangement, Which one occurs in an influenza major shift.
RNA segment rearrangement
this process describes when self-reactive T cells become nonreactive without costimulary molecule
anergy
can B cells become anergic
yes -but tolerence is lest complete than in T cells
this type of hypersensitivity involves aaphylactic and atopic reactions
Type I
Mneu: First and Fast (anaphylaxic)
In this type of hypersensitivity rxn the Ag cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines (i.e., histamine). A reaction develops rapildly after Ag exposure due to preformed Ab. E.g., include anaphylaxis, asthma, hives, local wheal and flare
Type I
This type of hypersensitivity is Ab mediated. IgM & IgG bind to Ag on “enemy” cell, leading to lysis (by complement or phagocytosis. E.g., include autoimmune hemolytic anemia, Rh dz(erythroblastosis fetalis), goodpasture’s syndrome, rheumatic fever, Graves dz, bullous pemphigoid, myasthenia gravis, ITP
type II
mneu: cy-2-toxic
In type II hypersensitivity rxns the Ab & complement lead to this complex
membrane attack complex
these types of hypersensitivity reactions are Ab mediated
I,II,III
Immune complex, serum sickness, and Arthrus reactions describe this type of hypersensitivity reaction
type III
In this subtype of a type III hypersensitivity reaction Ag-Ab complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes. Examples include PAN, immune complex glomerulonephritis, SLE,rheumatoid arthritis.
immune complex
immune complexes are essentially 3 things stuck together. What are they?
Ag-Ab-C’
pt presents with fever, uticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after Ag exposure
serum sickness
This subtype of a type III hypersensitivity reaction is an immune complex dz in which Ab to the foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes, where they fix compliment (leads to tissue damage).
Serum Sickness
most serum sickness is now caused by this not serum
drugs
This subtype of a type III hypersensitivity reaction is a local subacute Ab mediated hypersensitivity. Intradermal injection of Ag induces Ab, which form Ag-Ab complexes in the skin. It is characterized by edema, necrosis, and activation of complement. Examples include hypersensitivity pneumonitis (farmer’s lung) and thermophilic actinomycetes.
Arthrus reaction
these complexes cause the arthrus reaction
Ab-Ag complex
This type of hypersensitivity involves delayed (T cell mediated) reactions. Sensitized T lymphocytes encounter Ag and then release lymphokines which leads to macrophage activation
Type IV
mneu: 4th & last-delayed
Type IV hypersensitivity reactions are cell mediated–therefore are they transferable by serum
No
Give the 4 Ts of type IV hypersensitivity reactions
T lymphocytes, Transplant reactons, TB skin tests, Touching (contact dermatitis)
Use the ACID mneumonic for the types of hypersensitivity. . . .
A-Anaphylactic and Atopic(I)
C-Cytotoxic (Ab mediated[II]
I-Immune complex (III)
D-Delayed (cell mediated[IV]
Give the immune deficiency:
this is an X linked recessive defect in a tyrosine kinase gene associated with low levels of all classes of immunoglobins. It is Associated with recurrent BACTERIAL infections after 6 mo. of age, when levels of maternal IgG Ab decline. It occurs in BOYS (X-linked)
Bruton’s agammaglobulinemia (decreased production of B cells)
Give the immune deficiency:
This occurs when the THYMUS and paraTHYROIDS fail to develop owing to failure of development of the THIRD and fourth pharyngeal puches. It presents with TETANY owing to hypocalcemia. Pt often has recurrent viral and fungal infections due to T-cell deficiency. Congenital defects of heart and great vessels often accompany. There is a 22q11 deletion
Thymic aplasia (DiGeorge syndrome) decrease production of T cells
Give the immune deficiency:
This is a defect in early stem-cell differentiation. It presents with recurrent viral, bacterial, fungal and protozoal infections. It may have multiple causes (e.g., failure to synthesize MHC II Ag, defective IL-2 receptors or adenosine deaminase deficiency.
Severe combined immunodeficiency (SCID)
decreased production of B & T cells
Give the immune deficiency:
Pt presents with disseminated mycobacterail infections.
IL-12 receptor deficiency
T cell activation problem
Give the immune deficiency: Defect in the CD40 ligand on CD4 T helper cells leads to inability to class switch. Presents early in life with severe pyogenic infections. High levels of IgM; very low levels of IgG, IgA, & IgE
Hyper IgM syndrome
B cell activation problem
Give the immune deficiency:
X linked defect in the ability to mount an IgM response to capsular polysaccharides of bacteria. Associated with elevated IgA levels, normal IgE levels, and low IgM levels. Triad of symptoms includes recurrent pyogenic Infections, thrombocytopenic Purpura, Eczema (WIPE).
Wiskott-Aldrich Syndrome
B cell activation problem
Give the immune deficiency:
Failure of gamma-interferon production by helper T cells. Neutrophils fail to respond to chemotactic stimuli. Presents with recurrent “cold” (noninflamed) staphylococcal abscesses, eczema, coarse facies, retained primary teeth, and high levels of IgE
Jobs syndrome-
decreased activation of macrophages
Give the Immune deficiency:
Defect in LFA-1 adhesion proteins on phagocyts. Presents early with sever pyogenic and fungal infections and delayed seperation of umbilicus
Leukocyte adhesion deficiency syndrome
Phagocytic cell deficiency
Give the Immune deficiency: Autosomal recessive defect in microtubular fx and lysosomal emptying of phagocytic cells. Presents with recurrent pyogenic infxns by staphylococci and streptococci, partial albinism, and peripheral neuropathy
Chediak-Higashi dz
phagocytic cell deficiency
Give the Immune deficiency: Defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or similar enzymes. Presents with marked susceptibility to opportunistic infxns with bacteria, especially S. aureus, E. coli, and Aspergillus. Diagnosis is confirmed with negative nitroblue tetrazolium dye reduction test
Chronic granulomatous dz
phagocytic cell deficiency
Give the Immune deficiency:
T-cell dysfunction specificallly against Candida albicans. Presents with skin and mucous membrane Candida infections.
Chronic mucocutaneous Candidiasis-
Idiopathic dysfunciton of T cells
Give the Immune deficiency: Deficiency in a specific class of immunoglobulins--possibly due to a defect in isotype switching. Selective IgA deficiency is the most common selective immunoglobin deficiency. Presents with sinus and lung infections. Milk allergies and diarrhea are common.
Selective immunoglobin deficiency
Idiopathic dysfunction of B cells
Give the Immune deficiency:
Defect in DNA repearin enzymes with associated IgA deficiency. Presents with cerebellar problems (ataxia) and spider angiomas (telangiectasia.
ataxiatelangiectasia-
idiopathic dysfunction of B cells
Given the autoantibody, give the associated disorder: antinuclear Ab (ANA)
SLE
Given the autoantibody, give the associated disorder: Anti-dsDNA, anti-Smith
specific for SLE
Given the autoantibody, give the associated disorder:
Antihistone
drug induced lupus
Given the autoantibody, give the associated disorder: Anti-IgG (rheumatoid factor)
rheumatoid arthritis
Given the autoantibody, give the associated disorder: antineutrophil (C-ANCA, P-ANCA)
Vasculutis
Given the autoantibody, give the associated disorder: Anticentromere
Scleroderma (CREST)
Given the autoantibody, give the associated disorder:
Anti-Scl-70
Scleroderma (diffuse)
Given the autoantibody, give the associated disorder: antimitochondrial
primary biliary cirrhosis
Given the autoantibody, give the associated disorder: Antigliadin
Celiac dz
Given the autoantibody, give the associated disorder:
Anti-basement membrane
Goodpasture’s syndrome
Given the autoantibody, give the associated disorder:
Anti-epithelial cell
Pemphigus vulgaris
Given the autoantibody, give the associated disorder:
Antimicrosomal
Hashimoto’s thyritis
Given the autoantibody, give the associated disorder: Anti-Jo-1
polymositis, dermatomyositis
Hive the HLA subtype that coincides with the following disorders: Psoriasis, Ankylosing spondylitis, Inflammatory bowel dz, Reiter’s syndrome.
B27
mneu: PAIR
Give the HLA subtype which cooresponds to the following dz:
Graves’ dz, celiac sprue
B8
Give the HLA subtype which cooresponds to the following dz:
MS, hay fever, SLE, Goodpasture’s
DR2
Give the HLA subtype which cooresponds to the following dz: DM type I
DR3
Give the HLA subtype which cooresponds to the following dz:
Rheumatoid arthritis, DM type 1
DR4
Give the HLA subtype which cooresponds to the following dz: Pernicous anemia (B12 deficiency) Hashimoto's thyroiditis
DR5
Given the autoantibody, give the associated disorder:
Steroid-responsive nephrotic syndrome
DR7
This type of transplant rejection is Ab mediated due to presence of preformed antidonor Ab in the transplant recipient. It occurs within minutes after transplantation.
hyperacute rejection
This type of transplant rejection is cell mediated due to cytotoxic T lymphocytes reacting against foreign MHCs. It occurs weeks after transplantation. It is reversible with immunosuppressants such as cyclosporin and OKT3
Acute rejection
This type of transplant rejection is Ab mediated vascular damage (fibrinoid necrosis) it occurs months to years after transplantation. It is irreversible.
Chronic rejection
This type of transplant rejection happens when grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with “foreign” proteins, resulting in severe organ dysfunction. Major symtoms include maculopapular rash, jaundice, hepatosplenomegly, and diarrhea
Graft v. Host dz
This type of transplant rejection is Ab mediated vascular damage (fibrinoid necrosis) it occurs months to years after transplantation. It is irreversible.
Chronic rejection
This type of transplant rejection happens when grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with “foreign” proteins, resulting in severe organ dysfunction. Major symtoms include maculopapular rash, jaundice, hepatosplenomegly, and diarrhea
Graft v. Host dz
