Intro Immuno Flashcards
B Lymphocyte
Neutralization of microbe, phagocytosis, complement activation
Bruton’s Agammaglobulinemia
X-linked Deficiency: BTK
C-reactive protein (CRP)
Binds phosphocholine expressed on some bacteria and on dead/dying cells (opsonin), activates complement via C1Q complex leading to generation of C3b
C1 INH Deficiency
Results in hereditary angioedema Type I, (autosomal dominant) ROS: swelling, commonly face, lips, floor of mouth, throat, larynx
C1 Inhibitor (C1 INH)
Inhibits C1r and C1s serine protease activity
C1q
Binds to Ab that has bound Ag, thus allowing activation of C1r
C1r
Cleaves C1s to active protease
C1s
Cleaves C4 and C2
C2a
Precursor of vasoactive C2 kin in
C2b
Active enzyme of classical pathway C3/C5 convertase: cleaves C3 and C5
C3 Deficiency
Rare and associated w/ severe recurrent Neisseria infections and poor immune response in infancy, usually fatal
C3a
Stimulates inflammatory response
C3b
Binds to the surface of a microbe, where it functions as an opsonin and as a component of C3 and C5 convertases, binds C5 for cleavage by C2b
C4 Binding Protein (C4BP)
Causes dissociation of classical pathway C3 convertase subunits, is a cofactors for Factor I-mediated cleavage of C4b
C4a
Weak mediator of inflammatory response
C4b
Covalently binds to pathogen and opsonizes it, binds C2 for cleavage by C1s
CD59 (MAC inhibitory protein)
Blocks C9 binding and prevents formation of the MAC
CH50
Low levels of CH50 can be used to monitor progression of autoimmune or other dz (like SLE-lupus: low C3 and C4)
Common Variable Immunodeficiency (CVID)
Deficiency: CD19, CD20, BAFF-R
Cytotoxic T Lymphocyte (CTL)
Ag recognition: infected cell expressing microbial ag Killing of infected host cell
Decay Accelerating Factor (DAF)
Blocks formation of C3 convertase, prevents normal human host cells from activating the MAC
Factor B
Bb is a serine protease and the active enzyme of C3 and C5 convertases
Factor D
Plasma serine protease that cleaves factor B when it is bound to C3b
Factor H (complement)
Cofactor for Factor I-mediated cleavage of C3b, and causes dissociation of alternative pathway C3 convertase subunits
Factor I (complement)
Proteolytically cleaves C3b and C4b (inactivator) and produces C3d
Helper T Lymphocyte
Ag recognition: microbial ag presented by APC Activation of MAC, inflammation, activation (proliferation and differentiation) of T and B lymphocytes
Hyper-IgM Syndrome (HIGM2)
Deficiency: AID Effect: prevents class switch, limiting Ab production to low variability IgM
IFN-α / IFN-β
*Type I IFN Secreted by: dendritic cell, MAC Activity: target virally uninfected (neighboring) cells and inhibit viral replication and propagation, inc MHC-I expression, NK cells: activation
IFN-γ
*Type II IFN but Type I cytokine Secreted by: TH1, CTL, CD8+, NK Activity: - uninfected/MAC/phagocytic: inhibits viral replication, classic MAC activation - increases expression of MHC I and II - TH2: inhibits type II cytokines IL-4 and class switch to IgE and IgG1
IgA
In serum is monomer, but dimmer in secretions with secretory component and J chain associated, secretory piece is made in epithelial cells Function: local mucosal immunity, does not fix complement, can bind PMNs and induce phagocytosis
IgD
4th most abundant, found primarily on naive B cell surfaces, associates w/ CD79a and CD79b signaling molecules Function: receptor for Ag
IgE
Least abundant in serum,