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33 Cards in this Set

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  • Back
BAFF
Serves as signal 2 for marginal zone B cells (signal 1 = BCR binding antigen, with crosslinking).
C3a
Moderate chemokine - attracts macrophages and neutrophils.
Induces local inflammation - vasopermeability, mast cell degranulation and smooth muscle contraction.
Anaphylatoxin.
C3b
Opsonization.
Formation of active C3 convertase.
Formation of active C5 convertase.
C5a
Strong chemokine (stronger than C3a) - attracts macrophages and neutrophils.
Induces local inflammation - vasopermeability, mast cell degranulation and smooth muscle contraction.
Anaphylatoxin.
C5b
MAC formation (recruits C6/C7/C8/C9).
CCL18
Attracts T cells to dendritic cells in lymph nodes.
CCL19/CCL21
Attracts B cells and T cells to T cell zone of lymph nodes.
Binds CCR7.
CXCL13
Attracts naïve follicular B cells to B cell zone in lymph nodes.
Binds CXCR5.
CXCL8
Attracts neutrophils.
FoxP3
NOT A CYTOKINE, but important because natural Treg cells express it.
GM-CSF
Induces macrophage differentiation in bone marrow.
IFN-alpha (type 1)
Activates NK cells.
IFN-beta is activated first, IFN-alpha is activated later.
IFN-beta (type 1)
Activates NK cells.
IFN-beta is activated first, IFN-alpha is activated later.
IFN-gamma (type 2)
Activates macrophages.
Induces activated T cells to differentiate into TH1 cells (signal 3).
IL-10
Inhibits NK cells.
IL-12
Activates NK cells.
Induces activated T cells to differentiate into TH1 cells (signal 3).
IL-1beta
Causes fever.
Activates vascular endothelium.
Activates acute phase response (CRP and MBL).
Activates macrophages/neutrophils.
IL-2
Induces massive proliferation of activated T cells.
IL-3
Induces macrophage differentiation in bone marrow.
IL-4
Activates B cell differentiation into plasma cells.
Induces activated T cells to differentiate into TH2 cells (signal 3).
Production favors allergic response.
IL-5
Activates B cell differentiation into plasma cells.
Cause basophils/eosinophils to start expressing FC-epsilonRI and binding IgE on surface (in type 1 allergic response).
IL-6
Causes fever.
Activates vascular endothelium.
Activates acute phase response (CRP and MBL).
TNF-alpha
Causes fever.
Activates vascular endothelium.
Activates acute phase response (CRP and MBL).
Activates NK cells.
Causes dendritic cells to move to lymph nodes (adaptive response).
Type 1 interferons
Main antiviral cytokines. Include IFN-alpha and IFN-beta.
Production mediated via IRF-3.
Type 1 Hypersensitivity
Most important players are Th2 CD4s, mast cells, eosinophils, IgE, IL-4, IL-5, and IL-13. Most people will not have an immune response to innocuous substances (pollen, dust mite feces, nuts, etc). The first time the antigen is encountered, the person undergoes sensitization but does NOT have an allergic reaction.
Type II Hypersensitivity
Important players here are IgG (or sometimes IgM) antibodies that are produced to and bind to antigens on the surface of cells/tissues.
examples of Type 1 hypersensitity not considered autoimmune disease:
Common examples (not considered autoimmune disease) are:
--Penicillin-induced hemolytic anemia
--Hemolytic anemia caused by ABO-mismatched blood transfusions
--Erythroblastosis fetalis
--Hyperacute transplant rejection
examples of Type 1 hypersensitity - considered autoimmune disease:
Common examples of autoimmune diseases that are mediated by type II hypersensitivity:
--Autoimmune hemolytic anemia
--Idiopathic/autoimmune thrombocytopenia purpura
--Pernicious anemia
--Rheumatic fever (molecular mimicry causes antibodies produced in response to Strep infection to cross-react with self-antigens in heart, kidney, and joints)
--Goodpasture’s syndrome
--Graves’ disease
--Myasthenia gravis
--Bullous pemphigoid
--Pemphigus vulgaris
Type III Hypersensitivity
Important players here are IgG (or sometimes IgM or IgA) antibodies specific for soluble antigens. When these antibodies and antigens are found in an ~1:1 ratio in the serum, they form immune complexes which overwhelm clearance mechanisms in the spleen and can deposit on tissues throughout the body
examples of Type III Hypersensitivity not considered autoimmune disease
Common examples (not considered autoimmune disease) are:
--Arthus reaction (injection of antigen in individual with pre-existing antibodies can lead to formation of immune complexes and inflammation at site of antigen injection)
--Serum sickness (antibodies to foreign proteins in serum of transfused blood)
--Post-streptococcal glomerulonephritis (antibodies to Strep antigens form complexes and are deposited in kidney vasculature)
--Hypersensitivity pneumonitis (Farmer’s lung)
examples of Type III Hypersensitivity - considered autoimmune disease
Common examples of autoimmune diseases that are mediated by type III hypersensitivity:
--SLE (lupus)
--Polyarteritis nodosa (a type of vasculitis that is likely autoimmune)
--Rheumatoid arthritis has features of type III hypersensitivity (although in this class we are considering it to be type IV hypersensitivity)
example of Type IV Hypersensitivity (Delayed-type hypersensitivity) not considered autoimmune disease:
Common examples (not considered autoimmune disease) are:
--Poison ivy/oak (contact dermatitis): Poison ivy contains a hapten called pentadecacatechol
--Nickel (and other metal) “allergy” (these are more properly called contact dermatitis since they are type IV and not type I like true allergies): the small metal ions are haptens
--PPD skin test
--Guillain-Barré syndrome
--GVHD
--Acute transplant rejection
--Chronic transplant rejection (chronic rejection also involves antibody-mediated type II or type III hypersensitivity as well)
example of Type IV Hypersensitivity (Delayed-type hypersensitivity) - considered autoimmune disease:
Common examples of autoimmune diseases that are mediated by type IV hypersensitivity:
--Type I diabetes
--Multiple sclerosis
--Hashimoto’s thyroiditis
--Celiac disease (response to peptides derived from gluten such as gliadin)
--Rheumatoid arthritis (although it can involve immune complexes, not all patients have Rheumatoid Factor so it is more likely that it is the cellular infiltration of the joints that is causing the symptoms)

Treatment is disease-specific, but in many cases immunosuppression can be helpful.