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