Robbins Chapter 6 Key Concepts Flashcards
Receptor families used in innate immune system
Toll-like receptors that recognize microbes and damaged cells
What are the mediators of adaptive immunity
lymphocytes and are the only cells that produce specific and diverse receptors for antigens
Characteristics of T cells
have TCRs that recognize peptide fragments of protein antigens displayed on MHC cells of APCs
Characteristics of B cells
express antibodies that recognize antigens
Plasma cells
activated B cells that secrete antibodies
NK cells
kill cells that are infected by microbes
kill stressed or damaged cells beyond repair
express inhibitory receptors that recognize MHC on healthy cells so they don’t kill them
APCs function
capture microbes and transport them to lymphoid organs and display them for recognition by lymphocytes
Most efficient APC
dendritic cells which live in epithelia and most tissues
Generative lymphoid organs
bone marrow and thymus
production of mature lymphocytes
Peripheral lymphoid organs
lymph nodes, spleen, mucosal lymphoid tissues
where immune response occurs
Innate immunity components
epithelial barriers
phagocytes
NK cells
plasma proteins of complement system
Difference between innate immunity and adaptive immunity
innate is first response and doesn’t have fine antigen specificity or memory
adaptive develops slower but is more potent and specialized
Cell mediated immunity
reaction of T lymphocytes to fight cell-associated microbes
Humoral immunity
mediated by antibodies and is effective against extracellular microbes
Extracellular microbes
in circulation and mucosal lumens
Cell-associated microbes
phagocytosed microbes and microbes in cytoplasm of infected cells
CD4+ helper T cell function
help B cells make antibodies
activate macrophages to destroy ingested microbes
stimulate recruitment of leukocytes
regulate immune response to protein antigen
What mediates CD4+ T cells
cytokines
CD8+ cytotoxic T lymphocyte function
kill cells that express antigens in cytoplasm (virus and tumor cells) and can produce cytokines
Function of antibodies
neutralize microbes and block their infectivity
promote phagocytosis and destruction of pathogen
confer passive immunity to neonates
Other names for immediate (type I) hypersensitivity
allergic reactions or allergies
What induces immediate hypersensitivity?
environmental antigens (allergens) that stimulate strong Th2 responses and IgE production in genetically susceptible individuals
IgE functions
coats mast cells by binding Fce receptors
What are the principal mediators of immediate hypersensitivity
histamine, proteases, prostaglandins, leukotrienes, and cytokines
Function of the mediators of immediate hypersensitivity
immediate vascular and smooth muscle reactions and late-phase reaction (inflammation)
Functions of antibodies
opsonize (coat) cells and target them for phagocytosis
How do antibodies recruit phagocytes
phagocytes express receptors for Tc tail of IgG and complement proteins
Where do antibodies and immune complexes deposit?
tissues or blood vessels
Result of antibody and immune complex deposition
acute inflammation by activating complement or engaging Tc receptors on leukocytes
causes tissue damage
Cytokine-mediated inflammation process
CD4+ T cells activated by protein antigen and differentiate in Th1 and Th17 and activate IFNy to activate macrophages
Results of cytokine-mediated inflammation
tissue damage and promote fibrosis
IL-17 in cytokine-mediated inflammation
recruit leukocytes and promote inflammation
Classical T cell-mediated inflammatory reaction
delay type hypersensitivity
T-cell mediated cytotoxicity process
CD8+ cytotoxic T lymphocytes (CTLs) specific for antigen recognize and kill cell
also secrete IFNy
Immunologic Tolerance
unresponsiveness to self antigen
*fundamental property of the immune system
What happens in Central Tolerance
immature lymphocytes that recognize self antigens in the generative lymphoid organs are killed by apoptosis
What happens in Peripheral Tolerance
mature lymphocytes that recognize self antigens in peripheral tissues become functionally inactive, or are suppressed by regulatory T lymphocytes, or die by apoptosis
What 2 factors lead to failure of self-tolerance and the development of autoimmunity
- Inheritance of susceptibility genes
2. Infections and tissue injury that ay expose self antigens and activate APCs and lymphocytes in the tissue
Characteristics of autoimmune diseases
Chronic and progressive and tissue injury occurs
What causes SLE
autoantibodies produced against self antigens and formation of immune complexes
Role of autoantibodies in SLE
directed against nuclear antigens
Disease manifestations of SLE (5)
nephritis, skin lesions, arthritis, hematologic abnormalities, neurologic abnormalities
What causes arthritis in SLE
deposition of immune complexes
What causes the breakdown of self-tolerance in SLE (3)
nuclear antigens, genetic factors, environmental factors
What is Sjogren syndrome
inflammatory disease that affects salivary and lacrimal glands causing dryness of mouth and eyes
What causes Sjogren syndrome
autoimmune T-cell reaction against self antigens in the lacrimal and salivary glands
viral infection against infects the tissues
What characterizes Systemic sclerosis (scleroderma)?
progressive fibrosis involving skin, GI, and other tissues
How does fibrosis occur in systemic sclerosis
activation of fibroblasts by cytokines produced by T cells
How does the rejection response against solid organ transplants occur?
initiated by host T cells that recognize foreign HLA antigens of the graft
4 mechanisms of rejection of solid organ grafts
hyperacute, acute cellular rejection, acute humoral rejection, and chronic rejection
Hyperacute rejection of solid organ
preformed antidonor antibodies bind to graft immediately after transplant
Acute cellular rejection of solid organ
T cells destroy graft parenchyma by cytotoxicity and inflammatory reactions
Acute humoral rejection of solid organ
antibodies damage graft vasculature
Chronic rejection of solid organ
dominated by arteriosclerosis
caused by T cell activation and antibodies
vascular lesions and T cell reactions cause parenchymal fibrosis
Treatment of graft rejection
immunosuppressive drugs that inhibit immune responses against the graft
Diseases associated with HSC transplantation
graft vs host diseases, and immune deficiency
Primary inherited immune deficiency diseases
inherited mutations in genes involved in lymphocyte maturation or function or in innate immunity
Results of deficiencies in innate immunity
defects of phagocyte function, complement, and innate immune receptors
X-SCID cause
adaptive immunity problem
mutation in common y chain of cytokine receptor
X-SCID results
failure of T and B cell maturation
failure of IL-7 signaling
defective lymphopoiesis
Autosomal recessive SCID cause
secondary defect in antibody responses
mutation in gene encoding ADA
Autosomal recessive SCID results
failure of T cell development
accumulation of toxic metabolites during lymphocyte maturation and proliferation
X-linked Agammaglobulinemia cause
mutation in the BTK gene which encodes B cell tyrosine kinase that is required for maturation signals from pre-B cell and B cell receptor
X-linked Agammaglobulinemia results
failure of B-cell maturation
Common Variable Immunodeficiency result
defect in antibody production
X-linked hyper-IgM syndrome cause
mutation in gene encoding CD40L
X-linked hyper-IgM syndrome results
failure to produce isotype-switched high affinity antibodies IgG IgA and IgE
X-linked lymphoproliferative disease (XLP) cause
defect in a signaling molecule
X-linked lymphoproliferative disease (XLP) result
defective responses against Epstein-Barr virus and lymphoproliferation
