immunology Flashcards
site of B cell localization and proliferation
Lymph node follicle
active follicles
secondary
contain reticular cells and macrophages
lymph node medulla
houses T cells
lymph node paracortex
not well developed in Di George
lymph node paracortex
lymph drainage of upper limb and lateral breast
axillary
lymph drainage of stomach
celiac
lymph drainage of duodenum, jejunum
superior mesenteric
lymph drainage of sigmoid colon
colic –> inferior mesentaric
lymph drainage of rectum
internal iliac
lymph drainage of anus
superficial inguinal
lymph drainage of testes
superficial and deep plexuses –> paraaortic
lymph drainage of scrotum
superficial inginal
lymph drainage of thigh (superficial)
superficial inguinal
drained by right lymphatic duct
right upper quadrant - including right side of head
T cells found in ___ of spleen
periarterial lymphatic sheath
B cells found in ____ of spleen
follicles in the white pulp of spleen
macrophages in spleen remove
encapsulated bacteria
immune issues in splenic dysfunction
low IgM–> lower complement activation –> low C3b opsonization
encapsulated bugs a problem in spenic dysfunction
strep p HiB neissera meningitis salmonella Klebsiella Group B Strep
function of thymus
positive selection of T cells (cortex) negative selection (medulla)
neutrophils, macrophages, NK cells, and complement mediate
innate immunity
T cells, B cells and circulating antibody mediate
adaptive immunity
MHC I and II
encoded by HLA genes and present antigen fragments to T cells. Bind TCR
encoded by HLA A,B,C
MHC I
binds CD8
MHC I
mediates viral immunity
MHC I
antigen is loaded in RER
MHC I
encoded by HLA DR,DP, DQ
MHC II
binds CD4
MHC II
expressed only on antigen-presenting cells
MHC II
HLA-A3 disease
hemochromatosis
HLA-B27
Psorisis, ankylosing spondy, inflammatory bowel disease, reiter’s
HLA-DQ2/8
celiac
HLA-DR3
DM1, graves disease
HLA-DR4
RA, DM1
HLA-DR5
pernicous anemia, hashimoto’s thyroitis
enhance NK activity
IL-2/12 IFN-B/a
NK cell MOA
use perfornin and granzymes to induce apoptosis
NK cells attack
viral infected cells and tumor cells
induces NK cells to kill
exposure to nonspecific activation signal on target cell or to absence of class I target cell surface
good B cell function
make antibody opsonize bacteria neutalize viruses (IgG) activate complement (IgM, IgG) sensitive mast cells (IgE)
bad B cell functions
allergy (type 1 hypersensitivity) cytotoxic (type II hypersensitivity) immune complex (type III hypersensitivity) hyperacute and humorally mediated acute and chronic organ rejection
good T cell functions
CD4: help B cells make antibody and produce cytokines to ackivate other immune cells
CD8: kill virus-infected cells directly
bad T cell functions
delayed cell-mediated hypersensitivity (IV)
acture and chronuc cellular organ rejection
positive selection makes ____ cells survive
TCRs capable of binding surface self MHC
negative selection makes ___ cells DIE
TCRs with high affinity for self antigens
activates T cells
dendritic cells
macrophages
B cells
only APC that can activate naive T cell
dendritic
costimulatory signal activating naive T cells
B7 (on dendritic) and CD28 (on T cell)
receptor on B cell that binds to Th cell
CD40
secretes cytokines to determine class switching of B cells
T helper cell (CD4)
Th1 cell secretes
IFN-gamma
activates macrophages
Th1
inhibits Th1 cells
IL-4 and IL-10
secretes IL-4/IL-10
Th2
express CD4
Th1
Th2 cells secrete
IL-4/5/10/13
recruits eosinophils
Th2
inhibited by IFN-g
Th2
kills virus inducedm neoplastic and donor graft cells
cytotoxic T cells
MOA of
perforin and granzyme
cytotoxic cells express
CD8
express MHC 1
virus infected cell
express MHC II
B cells
supress CD4 and CD8 cells
regulatory T cells
express CD3/4/25
regulatory T cells
priduce IL-10 and TGF-B
regulatory T cells
function of IL-10 and TGF-B
antiinflamatory
“arms” of the antibody
Fab segment
“Tail” of the antibody
Fc segment
antigen binding fragment
Fab (VH/L)
determins indiotype
Fab
binds complement
Fc (CH2)
determins isotype
Fc
antibody promotes phagocytosis
opsinization
antibody promotes bacterial adherance
neutralization
enhaces lysis
membrane attack complex
generates antibody diversity
random recombination of VJ (light chain) and VDJ (heavy chain) genes
antibody toes that bind complement
IgG and IgM
IgG functions
fixes complement
crosses placenta
opsonizes bacteria
neutralizes bacterial toxins and viruses
main antibidy in delayed response to antigen
IgG
IgA function
prevents attachment of bacteria dn viruses to mucous membranes
found in secretions and colostrum
IgM function
produced in immediate response to atigen
fixes complement
antigen receptor on surace of B cells
shape of pentamer
IgE function
binds mast cells and basophils
cross-links when exposed to allergen
mediates type 1 hypersensitivity through relese of histamine
mediates immunity to worms by activating eosinophils
mediates classic complement pathway
IgG/IgM
mediates alternative complement pathway
microbe surface molecules
mediates anaphylaxis
C3a, C5a
activates neutrophil chemotaxis
C5a
activates MAC
C5b-9
mediates opsonins
C3b and IgG
inhibits complment from actiaving on self cells
Deleay accelrating factor (DAF)
C1
C1 esterase deficiency leads to
heriditary angioedema (contraindicates ACE inhibitor)
C3 deficiency leads tro
severe, recurrent pyogenic sinus and respiratory tract infections. higher susceptibility to type III hypersensitivty reactions
C5-C9 deficicncy leads to
recurrent neisseria bacteramia
DAF defiecny leads to
complement medated RBC lysis and paroxysmal nocturnal hemoglobinria
IL-1 function
FEVER, actute inflamation, a
IL-2 function
stimulates T cells
IL-3 dunction
stimulates bone marrow
IL-4 function
stmulates IgE function
IL-5 dunction
stimulates IgA function
Il-6 function
fever and production of acute-phase proteins
IL-8 function
major chemotactic factor for neutrophils (clean-up on aILse 8)
Il-12 function
differentates T cells into Th1 cells, activates NK cells, (also secreted by B cells)
TNF-alpha function
mediates septic shock, activates endothelim, vascular leack
secreted by macrophages
IL 1/6/8/12 tnf-alpha
secreted by all T cells
IL-2/3
secreted by Th1 cells
interferon gamma
function of interferon gamma
activates macrophages and Th1 cells, supreses Th2 cells, has antiviral/antitumor properties
secreted by Th2 cells
IL-4/5/10
function of IL-10
modulates inflammatory cells, regulator function
inhibit viral protein synthesis
interferon A and B
increase MHC I/II espxression and antigen presentation in all cells
interferon gamma
all cells (except RBC) express
MHC 1
T cells express
TCR, CD3, CD28
helper T cells express
CD4, CD40 ligand
cytotoxic T clls express
CD8
B cells express
Ig, Cd19, CD20, CD21, CD40, MHCII, B7
macrophages expressC
CD14, Cd40, MHCII, B7, Fc and C3b receptors
NK cells express
CD16, CD56
unique marker for NK
CD56
binds Fc of IgG
CD16
anergy
self-reactive T cells become nonreative without constimulatory molecule
effect of superantigens
cross-like the B region of the T cell receptor to the MHC II class II on APC. Can activate any T cells - leads to cytokine stomr
release superantigens
staph A, S pyogenes
undergo antigen variation
salmonella, borrelia (relapsing fever), neisseria gonorrhoea, flu virus, trupanosomes
Passive immunity comes from
recieving preformed antibodies
speed of passive immunity
rapid
how passive immunity can be induced
IgA in breast milk, antitoxin, humanized monoclonal antibody
examples of passive immunity medical therapy
botox, tetanus, rabies, or HBV post exposure vaccination of preformed antibodies
active immunity comes from
exposure to forigen antigens
speed of active immunity
slow
how active immunity can be induced
natural infection, vaccienes, toxoid
live vaxes
MMR, sabin polio, varicella, yellow fever
innactivated or killed vaxes
cholera, hep A, Salk polio, rabies
live vax induces a
cellular response
killed vax induces
humoral immunity
anyphlaxis is what of hypersensitivity
type 1
immune complexes are what of hypersensitivity
type III
serum sickness and arthus reaction is what of hypersensitivity
type III
antibody and complement is what of hypersensitivity
type II
delayed sensitivity is is what of hypersensitivity
type IV
cell mediated is is what of hypersensitivity
type IV
mostly local autoimmmunity diseases are what of hypersensitivity
type II
most systemic autoimmunity is what of hypersensitivity
type III
MS, GB and GVHD are what of hypersensitivity
type IV
anticentromere antibody gives
scleroderma (CREST)
anti-basement membrane antibody gives
goodpastures
anti-desmolgein antibody gives
pemphigus vulgaris
antithyroglobulin antibody gives
hashimoto’s
asnti-SSA/SSB antibody gives
sjogren’s
anti-glutamate decarboxylase antibody gives
DM 1
c-ANCA antibody gives
Wengerner’s granulomatosis
p-ANCA antibody gves
microscopic polyangiitis, churg-strauss syndrome
if you don’t have T cells you’ll get
sepsis, CMV, EBV, ZVZ, chronic viral RTI, candida and PCP (think AIDS)
if you don’t have B cells you’ll get
encapulated bacteria infections (SHiN SKiS)
entoviral encephilitis, polio
GI giardiasis
if you don’t have granulocytes you’ll get
staph, serratia, nocardia, candida, aspergilus
if you don’t have complement you’ll get
neiserria (because of no MAC)
X linked (burton’s aggammglobulinemia) defect/presentation
defect in BTK - no B cells
recurrent bacteria after 6 months
selective IgA deficeicy defect/presentation
unknown (but most common)
majority asymptomatic, but can see autoimmune and anaphylaxis to IgA products
common variable immunodeficnecy defect/presentation
defect in B cell maturations due to multiple causes. results in normal B cells, but low # of plasma cells and immunoglobulin
aquired in 20-30s, high risk of autoimmune, lymphoma, sinopulmonary infection
DiGeorge defect/presentation
22q11 deletion. failure to develop 3/4 pharyngeal pouches
tetany, recurrent viral/fungal infections. Congenital heart defects
Hyper-IgE (Job’s syndrome) defect/presentation
Th1 cells fail to produce IFN-g (inability of neutrophils to respond to chemotaxis)
coarse facies, abcesses, retained primary teeth, eczema
SCID defect/presentation
commonly X linked, defective IL-2 receptor , adenosine deanimase deficnecy
failure to thrive, chronic diarrhea, thrush and lots of varied infections. No thymic shadow/germinal centers/B cells
treatment for SCID
bone marrow transplant (no allograft rejection)
ataxia-telengiectasia defect/presentation
defect in ATM gene, coding for DNA repair enzymes
ataxia, spider angiomas, IgA deficiency
Hyper IgM syndrome defect/presentation
CD40L on helper T cells defective - can’t class switch. almost no antibodies other than IgM
severe early life pyrogenic infections
wiskott-aldrich syndrome defect/presentation
X lnked. defective in WAS gene on X chromosome (high IgE/A, low IgM)
Thrombocytopenic purpua, infections and eczema
leukocyte adhesion deficncey defect/presentation
defect in LFA-1 integrin (CD18) on phagocytes - neutophilia
recurnednt bacterial infections, absent pus, delayed seperation of ummbilical cord)
chediak higashi syndrome defect/presentation
AR - defect in lysosomal trafficking regulator gene - microtubule dysfunction in phagosome-lysosome fusion
recurrent staph/stprep infection. partial albinism, peripheral neuropathy
chronic granulomatous disease defect/presentation
lack of NADPH oxidase –> sbsent respiratory burst in neutrophils
lots of catalase + infections (Staph, E colo, aspergillis)
allograft is from
self
syngenic graft from
twin or clone
allograft from
nonidentical individual of same species
xenograft from
different species