NKT cell surface receptor
Suppressor T-cells
(pan T-markers, receptor/s)
Helper T-cell
(receptor/s)
TH1
(antibody, action, secretion)
TH2
(antibody, action, secretion)
B-cell receptor
(for maturation and secretion of Ig)
NK cell
(surface markers, receptor/s)
pan B marker
indicates B lymphoid lineage
(marker)
pan T-cell Ab
most specific markers for T-cells
TCR: recognize peptide antigens
displayed by MHC
TCR: invariant; involved in transduction
TCR: recognize peptides, lipids, small molecules, w/o requirement
for display by MHC
promote B cell switching to
plasma cells to produce IgE;
further activation of more
CD4+ cells to become TH2 cells
(interleukin?)
most potent eosinophil activator
(interleukin?)
aids in IgE production
(interleukin?)
HLA-B27
HLA-B8
HLA-DR2
HLA-DR3
HLA-DR4
HLA-DR5
HLA-DQ3
graft rejection: preformed antibody
causing immediate vascular injury
via ADCC
graft rejection: days, months, years later; via T-cell mediated cytotoxic damage
kidney rejection:
early: subendothelial inflamm & hypertrophy of endothelium;
intermediate: moderate intimal prolif.
w/ more significant wall inflamm;
severe: significant fibrinoid
necrosis & intimal prolif.;
via cell-mediated & humoral immunity
kidney rejection: intimal fibrosis w/ vascular thickening; mononuclear infiltrates w/ prominent plasma cells; hyalinized stroma;
both T-cell and humoral mechanisms
cell necrosis of skin & GIT, cholestasis
(phase of GVHD)
over 100 days post-transplant dermal fibrosis, desquamative esophagitis, portal tract fibrosis, cholestasis
(phase of GVHD)
organs prominently involved in GVHD
marked cholestasis,
yellow-green bile pigment;
jaundice, fine scaling rash,
vacuolization of epidermal cells
most common cause for liver transplantation in children
Histocompatability required
in what organs?
w/in 2mos; mixed inflammatory portal
and central vein infiltrates
(liver rejection)
continued inflammation, portal fibrosis, arteriolar thickening, bile ductular necrosis
(liver rejection)
heart transplant:
lymphocytic infiltrates,
possible myocardial fiber necrosis
heart transplant: immunoglobulin deposition in small arteries = vasculitis
rim pattern fluorescence
speckled pattern fluorescence
nucleolar pattern fluorescence
centromere pattern fluorescence
SLE antibodies
Drug-induced SLE antibody
Sjörgen's Syndrome antbody
PSS Antibody
Polymyositis Antibody
MCTD antibody
malar skin rash, discoid skin rash, photodermatitis, serositis, glomerulonephritis, cytopenias, arthralgias, myalgias, vasculitis, dec C1q, thrombosis
genes associated w/ SLE
drugs that can produce SLE
skin plaques w/ varying degrees of edema, erythema, scaliness, follicular plugging, skin atrophy surrounded by elevated erythematous border;
usually affect face and scalp;
no renal involvement
SLE: what part of the skin is involved?
skin: chronic inflammatory infiltrates,
vasculitis, vacuolization and
dissolution of epidermis,
purpura w/ RBC extravasation
into upper dermis
SLE: immune complexes seen in dermal epidermal junction?
vascular thrombosis in dermis;
in vitro: interfere w/ coagulation;
in vivo: hypercoagulable, recurrent arterial & venous thrombosis, fetal loss
APS: autoantibodies directed against?
glomerulus: thickened capillary loops, "wire loop" capillaries, surrounding renal tubules are unremarkable
high titers of antibodies to ribonucleoprotein particle-containing U1 ribonucleoprotein
modest renal involvement, pulmonary hypertension, interstitial lung disease;
overlap of SLE, scleroderma, polymyositis
calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangectiasis; associated malabsorption -> riboflavin deficiency -> cheilosis
renal arterial intimal thickening and proliferation; hyperplastic arteriosclerosis -> malignant HPN w/ arterial fibrinoid necrosis, thrombosis & renal infarction
diffuse alveolar fibrosis
= honeycomb fibrosis;
morphea
symmetrical inflammation of
skeletal muscle w/ weakness;
skin rash; heliotropic rash
fibrosis of lacrimal and salivary gland, xerostomia
lacrimal and salivary gland
inflammation of any cause
failure of B cell precursors to develop into mature B cells
inheritance of Bruton's Disease
Bruton's Disease:
genetic defect involved?
affect production of?
absent B-cells, intact T-cell immunity;
multiple infections w/ bacterial organisms;
not apparent until about 6mos
normal numbers of circulating B cells; hyperplastic germinal centers;
NO plasma cells
impaired secretion of on or more Ig
(usually IgG, IgA); selective abnormality of
T cell activation (dec synthesis of IL-2, 4, 5)
dec. in CD4 cells or increase in CD8 cells; presence of T and B cell autoantibodies
genetic defect in DiGeorge Syndrome
field defect of 3rd and 4th pharyngeal pouch development in utero
total absence of thymic tissue; hypocalcemia, seizures
slight dec. in peripheral T cells; inc. infections but w/ less frequency and severity;
hypocalcemia, seizures
very little serum IgG, virtually no IgM or IgA
defect in X-linked SCID: mutation?
Autosomal Recessive SCID: defect?
infants develop: candidiasis, persistent diarrhea, severe respi tract infection w/ Pnuemocystis carinii, Pseudomonas, failure to thrive after 3mos
inheritance of Wiskott-Aldrich Syndrome?
thrombocytopenia, eczema,
dec IgM, inc IgA & igE;
T-cells: cytoskeletal disorganization, loss of microvilli, little CD43
genetic defect in Ataxia Telangiectasis?
inheritance of Ataxia Telangiectasia
progressive cerebellar ataxia, mucocutaneous telangiectasia,
recurrent respi tract infection
lack circulating and secretory IgA; impaired survival of IgA producing plasma cells
develop anti-IgA antibodies of the IgE type
giant cytoplasmic granules; leukopenia
(what disorder? inheritance?)
defect in Chronic Granulomatous Disease?
macrophage-rich chronic inflammatory reaction; susceptibility to
catalase-positive agents
profound suppression of T-cell mediated immunity, opportunistic infection, secondary neoplasm, neurologic disease
major targets of HIV infection
lymphopenia, dec T cell function in vivo & vitro, polyclonal B cell activation, altered monocyte/macrophage function
Viremia; sore throat, myalgias, fever, rash, weight loss, fatigue, cervical adenopathy, diarrhea, vomiting; resolves spontaneously
(what phase?)
persistent lypmhadenopathy w/ fever, rash, fatigue; period of clinical latency
(what phase?)
fever of more than 1 month duration, fatigue, weight loss, diarrhea, serious opportunistic infection, secondary neoplasms, clinical neurologic disease
(what phase?)
CDC HIV: Category 1
CDC HIV: Category 2
CDC HIV: Category 3
