Defense II Flashcards
natural innate immunity
1) omnipresent and never changing
antibody
1) IgM
- first antibody released into circulation
2) IgG
- major antibody of immune response
3) IgE
- found on the surface of the mast cells
- mediates hypersensitivity reaction
4) IgA
- milk, saliva, and tears
5) IgD: bound on B cells and rarely released into circulation
acquired adaptive immnity
1) adapts over time
2) humoral and cellular
T lymphocytes
1) characterized by expression of specific surface markers
- CD3 on all T cells (transduction of signals after antigen has been bound)
- CD4 helper T cells (cytokines)
- CD8 cytotoxic T cells (cell-mediated immunity)
2) mediators of innate immunity
- 60-70% of circulating lymphocytes
- recognize cell-bound antigen by means of antigen-specific TCR
TCR
1) heteroreceptor
2) antigen is bound
3) contains Cd3
B lymphocytes are
1) 10-20% of circulating lymphocytes
2) mediators of humoral immunity and secrete Igs
3) IgM is on all B cells for antigen receptor
4) CD20 and CD21 are expressed on B cells
natural killer cells
1) 10-15% of circulating lymphocytes
2) abundant granules to lyse tumor cells and virally infected cells without previous sensitization
3) CD16 represents Tc receptor for IgG and allows NK to lyse them!!
4) antibody dependent cell mediated cytotoxicity
5 )do not kill normal cells because they have self class I molecules
macrophages
1) mononuclear phagocytic system
2) required to process and present antigen to T cells
- class II MHC
3) produce cytokines that influence B and T cells
4) lyse tumor cells and secrete toxic metabolites
dendritic cells
1) located in lymphoid tissue
langerhans cells
1) in the epidermis
2) both have large amounts of class II molecules on their surface
3) present antigens to T cells
cytokines
1) protect against viral infections
- non specific inflammatory response
2) regulate lymphocyte growth
3) activate other inflammatory cells
4) chemotaxis of WBC
5) stimulate hematopoiesis with CSF
major histocompatibility complex
1) class I
- on all nucleated cells and platelet
- involved with action of cytotoxic T-lymphocytes CD8+
2) class II (HLA-D)
- antigen resenting cells (macrophages and dendritic cells
- involved in the pathway to specific immune response
- CD4+
remember 8
1) MHC 1 to CD8+
2) MHC 2 to CH4+
immune mechanisms and tissue damage
1) all can cause damage
2) hypersensitivity reaction
- usual or normal response to antigen can cause it
type I anaphylactic shock is
1) reaction within minutes after exposure to antigen (immediate hypersensitivity)
2) localized or systemic
3) vasoactive amines and things from mast cells
4) IgE
5) allergen => B cells make IgE => igE binds mast cells and basophils => reexposure causes binding again and initiation of reaction with POWERFUL mediators
systemic anaphylaxis
1) begins with itching and hives followed by respiratory difficulty (constriction of bronchioles)
- can have upper airway obstruction
- can be fatal within minutes
local reactions
1) atopic = hereditary
2) occur on skin or mucosa
3) fever, bronchial asthma, gastroenteritis
4) several parasitic infections => IgE
type II antibody mediated type
1) complement mediated
- Abs react with cell surface Ag
- complement causes cell lysis
- RBC commonly damaged
2) IgG or IgM against normal cell tissue
- Ags are intrinsic to the cell or tissue damaged
–
1) antibody dependent cell mediated cytotoxicity
- cell types that bear Fc portion of IgG cause lysis of target cells coated with it
- not phagocytosis or complement
2) antibody mediated cellular dysfunction
- Abs directed against cell surface receptors
- noncytotoxic but impair function
- grave’s disease
target cells
1) Ab will attach to NK => lysis
or
2) Ab recognize acetylcholine receptor and doesn’t allow the impulse to happen
type III immune complement mediated
1)Ag- Ab produce tissue damage by activation of serum mediators
2) activation of complement and accumulation of PMNs
3) effect on kidneys
- lupus
systemic immune complex disease (type iii)
1) formation of immune complexes against endogenous or exogenous Ags
- deposit of complexes in tissue
- neutrophil recruitment
2) acute and self-limiting
- fever, arthralgia, and acute necrotizing vasculitis and ischemic necrosis
- kidneys, joints
3) chronic disease develops with persistent or repeated exposure to Ag
- SLE and rheumatoid arthritis
local immune complex disease (type iii)
1) arthus reaction
2) local tissue necrosis from immune complex vasculitis
3) similar to systemic form
- necrotizing vasculitis and neutrophil accumulation
type IV cell mediated hyper sensitivity reaction
1) delayed hypersensitivity
2) CD4 t cells exposure to Ags bound to self MHC molecules
3) attracts macrophages and induced inflammation
-POISON IVY
- granulomas
4) T-cell mediated cytotoxicity
5) perivascular cuffing of monocytes and lymphocytes which leads to vascular permeability with edema and fibrin
6) caused by persistent and non-degradable Ags
type IV cell mediated cytotoxicity
1) Mediated by CD8 cells which kills Ag bearing target cells
2) Clas 1 MHC bind to and present Ag to t hese cells
- graft rejection
3s)CTL secrete molecules which drill holes in target cells causing apoptosis
