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266 Cards in this Set
- Front
- Back
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Lymph nodes
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secondary lymphoid organ
many afferents, 1 or more efferents encapsulated trabeculae filters macs stores and activates B and T cells produces antibodies |
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Lymph node follicle
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B cell localization and proliferation
outer cortex primary: dense and dormant secondary: active, pale central germinal centers |
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Lymph node medulla
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medullary cords
medullary sinuses |
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Lymph node
Medullary sinuses |
communicate with efferent lymphatics
contain reticular cells and macs |
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Lymph node
Medullary cords |
lymphocytes
plasma cells |
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Lymph node paracortex
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T cells
region of cortex between follicles and medulla enlarges during viral response high endothelial venules (B and T cells enter here from blood) *underdev in DiGeorge |
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Upper limb and breast lymph drainage
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axillary
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stomach lymph drainage
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celiac
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duodenum and jejunum lymph drainage
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Superior mesenteric
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sigmoid colon lymph drainage
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colic -> inferior mesenteric
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rectum lymph drainage (lower part), anal canal above pectinate line
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Internal iliac
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anal canal below pectinate line lymph drainage
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Superficial inguinal
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testes lymph drainage
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superficial and deep plexuses--> para aortic
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scrotum lymph drainage
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superficial inguinal
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thigh (superficial) lymph drainage
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superficial inguinal
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lateral side of dorsum of foot lymph drainage
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popliteal
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right lymphatic duct drains what?
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right arm and right half of head
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thoracic duct drains what?
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everything but right arm and right half of head
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Sinusoids of spleen
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long vascular channels in red pulp with fenestrated barrel hoop basement membrane
macs are found nearby |
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Where in the spleen are T cells?
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Periarterial lymphatic sheath (PALS)- around the central arteriole
red pulp |
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Where in the spleen are B cells?
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follicles in white pulp
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What do macs do in the spleen?
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remove encapsulated bacteria
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What is found in the red pulp of the spleen?
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T cells
RBCs |
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What happens with low IgM?
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low complement activation -> low C3b opsonization -> suscep to encapsulated bacteria
(S pneum, H. inf, salmonella) |
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Postsplenectomy features
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Howell-Jolly bodies (nuclear remnants)
target cells thrombocytosis |
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Thymus
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T-cell diff and maturation
encapsulated from epithelium of 3rd branchial pouches |
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Thymus cortex
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immature T cells
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Thymus medulla
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pale with mature T cells
epithelial reticular cells Hassalls corpuscles |
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Where do positive (MHC restriction) and negative (nonreaction to self) selection occur?
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Corticomedullary junction of thymus
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Where is the site of B cell maturation?
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Bone Marrow
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innate immunity
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receptors that recognize pathogens are germline encoded
fast nonspecific response, no memory Neutrophils, macs, dendritic cells, NK, complement |
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adaptive immunity
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receptors that recognize pathogens undergo V(D)J recombination during lymphocyte dev
Slow response with first exposure memory response is faster T, B, circulating antibody |
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Differentiation of T cells starts where?
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Bone marrow:
T cell precursor |
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After the bone marrow, T cell differentiation continues where?
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Thymus:
T cell in the cortex expresses both CD4+CD8+ In the medulla T cells express only one! |
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After the thymus, T cell differentiation occurs where?
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Lymph node:
T cells become either Helper T cells or cytotoxic T cells, |
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Helper T cell and IL-12 ---->
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Th1 cell
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Th1 cells make what?
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IL-2, IFN-gamma
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Th1 cells activate what?
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activate macs and CD8+ T cells
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Th1 cells are inhibited by?
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IL-10
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Helper T cell and IL-4 ---->
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Th2 cells
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Th2 cells make what?
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IL-4, IL-5, IL-10
help B cells make antibody (IgE > IgG) |
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Th2 cells are inhibited by
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IFN-gamma
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What is MHC?
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major histocompatibility complex?
encoded by Human Leukocyte Antigen (HLA) genes |
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What genes encode MHC1?
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HLA-A, B, C
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What expresses MHC1?
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almost all nucleated cells
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How is antigen presented on MHC1?
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antigen is loaded in RER of intracellular peptides
pairs with Beta 2 microglobulin which aids in transport to the surface |
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What genes encode MHC2?
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HLA-DR, DP, DQ
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What expresses MHC2?
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APCs
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How is antigen presented on MHC2?
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loaded following the release of invariant chain in an acidified endosome
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B cell function
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makes antibody
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IgG role
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opsonizes bacteria
neutralizes viruses |
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Cytotoxic type II hypersensitivity is Ig-?
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IgG
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Immune complex type III hypersensitivity is Ig-?
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IgG
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Allergy type I hypersensitivity is Ig-?
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IgE
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hyperacute organ rejection
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antibody mediated
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CD4+ T cell function
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help B cells make antibody
produce gamma interferon (activates macs) |
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CD8+ T cell function
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kill virus infected cells directly
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Delayed cell mediated hypersensitivity (type IV)
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T cells
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acute organ (allograft) rejection
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T cells
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chronic allograft rejection
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T cells
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Natural killer cells:
Use what? Kill how? |
perforin and granzymes
induce apoptosis of virally infected cells and tumor cells |
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What is the only lymphocyte member of innate immune system?
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NK cells
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What enhances NK activity
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IL-12, IFN-beta, IFN-alpha
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When do NK cells kill?
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when exposed to a nonspecific activation signal on target cell and/or absence of MHC 1
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Helper T cell glycoprotein
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CD4+ (binds MHC II on APC)
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Cytotoxic T cell glycoprotein
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CD8+ (binds MHC I on virus infected cell)
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CD3 complex
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cluster of polypeptides associated with T cell receptor
(important in signal transduction) |
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APCs
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mac
B cell dendritic cell |
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lymphocytes release what to stimulate macs?
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IFN-gamma
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macs release what to stimulate lymphocytes?
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IL-1, TNF-alpha
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What happens when B cell encounters a virus?
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IgM binds virus
B cell becomes plasma cell plasma cell becomes antibody |
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What happens when APC encounters virus?
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1.APC releases IL-1 and TNF-alpha
2.this recruits helper T 3.TCR on helper T binds MHC II on APC (APC presents viral antigen on MHC II) 4.helper T releases things that recruit B, cytotoxic T, more helper Ts, and APCs |
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What does helper T release to recruit APCs?
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IFN gamma
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What does helper T release to recruit cytotoxic Ts?
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IL-2, IFN gamma
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What does helper T release to recruit B cells?
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IL-4, IL-5
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What does helper T release to recruit more helper Ts?
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IL-2
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What does APC release to recruit helper T?
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IL-1, TNF alpha
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What happens when cytotoxic T encounters a virus?
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1. Virus has MHC 1
2. TCR on cytotoxic T binds MHC I |
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What do Superantigens do?
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S aureus and S pyogenes
1.crosslink beta region of TCR to the MHC II on APCs 2. results in uncoordinated release of IFN gamma from Th1 cells and release of IL6,IL1, TFNalpha from macs |
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What do endotoxins (LPS) from gram negative bacteria do?
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stimulate macs by binding to endotoxin receptor CD14
Th cells are not involved. |
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How many signals are needed for T cell activation?
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2
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How many signals are needed for B cell activation?
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2
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Th activation? 4 steps
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1. foreign body phagocytosed by APC
2. antigen presented on MHC II and recognized by TCR on Th (signal 1) 3. costimulatory signal is the interaction between B7 on APC and CD28 on Th 4. Th is activated to produce cytokines |
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Tc activation? 2 steps
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1. endogenously synthesized (viral or self) proteins are presented on MHC I and recognized by TCR on Tc (signal 1)
2. IL2 from Th activates Tc to kill infected cell (signal 2) |
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B cell class switching? 2 steps
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1. IL4, IL5, IL6 from Th2 (signal 1)
2. CD40 receptor activation by binding CD40 ligand on Th cell (signal 2) |
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Which part of antibody recognizes antigen?
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variable part of L and H chain
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Which part of antibody fixes complement?
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Fc of IgM and IgG
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Heavy chain of antibody
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contributes to Fc and Fab
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Light chain of antibody
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contributes to Fab only
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Fab region
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antigen binding
determines idiotype |
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Fc region
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constant
carboxy terminal complement binding (IgG and IgM only) Carbohydrate side chain determines isotype |
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opsonization
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antibody promotes phagocytosis
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neutralization
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antibody prevents bacterial adherence
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complement activation
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antibody activates complement
enhances opsonization and lysis |
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antibody diversity:
4 ways |
1. random recomb of VJ (light) and VDJ (heavy) genes
2. random comb of heavy and light 3. somatic hypermutation after antigen stimulation 4. addition of nucleotides during recombination by terminal deoxynucleotidyl transferase |
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Immunoglobulin isotypes
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IgM
IgG IgA IgE IgD |
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Mature B lymphocytes express
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IgM and IgD
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How do B lymphocytes differentiate?
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isotype switching into plasma cells that secrete IgA, IgE, or IgG
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What is isotype switching
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alternative splicing of mRNA
mediated by cytokines and CD40 ligand |
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IgG
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main antibody in secondary response
most abundant fixes comp crosses placenta opsonizes bacteria neutralizes bacterial toxins and viruses |
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IgA
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prevents attachement of bact and virus to mucous membranes
does not fix comp monomer or dimer found in secretions |
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IgM
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primary response to antigen
fixes comp does not cross placenta receptor on B cells monomer or pentamer |
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IgD
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unclear function
on B cell surface |
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IgA
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type 1 hypersensitivity response
induces mast cell and basophils to release mediators mediates immunity to worms by activating eosinophils lowest concentration in serum |
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allotype
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Ig epitope that differs among members of same species
Can by on light or heavy chain different alleles (polymorphism) (in other words, different IgG alleles but still IgG) |
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isotype
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IgA vs. IgM etc
Epitope common to a single class of Ig determined by heavy chain |
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idiotype
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specific for a given antigen
Ig epitope determined by antigen binding site hypervariable region is unique |
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thymus independent antigens
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antigens lacking a peptide component
cannot be presented by MHC to T cells (LPS from cell env of gram neg bacteria) (polysaccharide capsular antigen) **stimulate release of IgM only and no memory!! |
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thymus dependent antigens
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contain a protein component (Hib vacc)
class switching and memory occur due to direct contact of B with Th cells (CD40 receptor ligand interaction) and release of IL4,5,6 |
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IL-1 is secreted by
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macs
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IL-1 role
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acute inflammation
recruits leukocytes activates endothelium to express adhesion molecules an endogenous pyrogen |
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IL-2 is secreted by
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Th cells
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IL-2 role
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stimulates growth of Th and Tc cells
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IL-3 is secreted by
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activated T cells
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IL-3 role
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growth and differentiation of bone marrow stem cells
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IL-4 is secreted by
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Th2
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IL-4 role
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promotes growth of B cells
enhances class switching to IgE and IgG |
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IL-5 is secreted by
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Th2
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IL-5 role
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promotes differentiation of B cells
class switching to IgA |
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IL-6 is secreted by
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Th2 and macs
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IL-6 role
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stimulates production of acute phase reactants and immunoglobulins
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IL-8 is secreted by
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macs
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IL-8 role
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major chemotactic factor for neutrophils
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IL-10 is secreted by
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regulatory T cells
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IL-10 role
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inhibits actions of activated T cells
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IL-12 is secreted by
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B cells
macs |
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IL-12 role
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activates NK and Th1 cells
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gamma interferon is secreted by
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Th1
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gamma IFN role
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stimulates macs
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TNF is secreted by
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macs
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TNF role
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septic shock
leukocyte recruitment vascular leak |
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helper T cells cell surface proteins
5 |
CD4, TCR, CD3, CD28, CD40L
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Cytotoxic T cell surface proteins
3 |
CD8, TCR, CD3
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B cell surface proteins
7 |
IgM
B7 CD19 CD20 CD21 (EBV receptor) CD40 MHC II |
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Macs cell surface proteins
6 |
MCH II
B7 CD40 CD14 Fc receptor C3b receptor |
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NK cell surface receptors
3 |
MHC I
CD16 (binds Fc of IgG) CD56 |
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all cells except mature rbc
cell surface protein |
MHC I
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Complement
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system of proteins that interact to play a role in humoral immunity and inflammation
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Membrane attack complex
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defends against gram negative bacteria
1. activated by IgG or IgM in classic path 2. activated by molecules on surface of microbes (endotoxin) in alternative pathway |
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What are the primary opsonins in bacterial defense?
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IgG
C3b- aids in clearance of immune complexes |
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Decay accelerating factor DAF
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prevents complement activation on self cells
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C1 esterase
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prevents complement activation on self cells
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C1,C2,C3,C4 role
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viral neutralization
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C3b role
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opsonization
binds bacteria |
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C3a, C5a role
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anaphylaxis
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C5a role
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neutrophil chemotaxis
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C5b-9 role
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MAC
cytolysis |
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Deficiency of C1 esterase
|
hereditary angioedema
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Deficiency of C3
|
sever recurrent pyogenic sinus and resp infections
inc susceptibility to type III HS reactions |
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Deficiency of C5-C8
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Neisseria bacteremia
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Deficiency in DAF (GPI-anchored enzyme)
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complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria (PNH)
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classic complement pathway
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antigen-antibody complex binds C1q->
C1r-> C1s -> cleaves C2 and C4 -> C2b4b (C3 convertase) -> C3 -> C3a + C4b,2a,3b (C5 convertase) -> C5 -> C5a + C5b -> C5b +C6 + C7 + C8 + C9 = MAC |
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lectin pathway
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microbial surface ->
mannan binding lectin -> protease cleaves C2 and C4 -> C2b4b -> C3 ... same as classical now! |
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alternative pathway
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microbial surfaces (endotoxin) ->
C3 + B + D --> C3bBb (C3 convertase) --> C3 --> C3b,Bb,C3b + C3a (C5 convertase) --> C5 --> same as classic now! |
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Interferons
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alpha, beta, gamma
proteins that place uninfected cells into antiviral state |
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Interferon mechanism
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induce production of ribonuclease that inhibits viral protein synthesis by degrading viral mRNA but not host mRNA
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alpha and beta IFN
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inhibit viral protein synthesis
activates NK cells to kill virus infected cells |
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gamma IFN
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increases MHC I and II expression and antigen presentation in all cells
activates NK cells |
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active immunity
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induced after exposure to foreign antigens
slow onset long lasting memory |
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passive immunity
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receiving preformed antibodies from other host
rapid onset, short life span (IgA in breast milk) |
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Preformed antibodies are given after exposure to what?
4 |
Tetanus toxin
Botulinum toxin HBV Rabies |
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Which bacteria have antigen variation?
|
salmonella (2 flagellar variants)
borrelia (relapsing fever) Neisseria gon (pilus protein) |
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Which virus has antigen variation?
|
Influenza
major -shift minor -drift |
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Which parasite has antigen variation?
|
trypanosomes (programmed rearrangement)
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anergy
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self reactive T cells become nonreactive without costimulatory molecule
(b cells can also do this but tolerance is less complete than in T cells) |
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Granulomatous diseases
9 |
1. TB
2. Crohns 3. sarcoidosis 4. Wegeners (necrotizing) 5. Fungi- blasto,crytpo, histo, coccido 6. leprosy 7. Cat scratch fever 8. Berylliosis 9. Syphilis |
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Granuloma mechanism
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1. APC binds Th cell
2. Th cell releases IFN gamma 3. monocyte -> macrophage -> epithelioid cell --> giant cell 4. Epithelioid cell + giant cell +fibroblasts + lymphocytes = granuloma |
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Type 1 HS
|
anaphylactic
atopic antibody mediated first fast |
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Type 1 HS mechanism
|
free antigen cross links IgE on mast and basophils, releasing histamine and other vasoactive amines that act on postcapillary venules
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Type 1 HS test
|
scratch test
radioimmunosorbent assay |
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Type II HS
|
IgM or IgG antibody mediated
complement mediated leads to MAC Cytotoxic (cy-2-toxic) |
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Type II HS mechanism
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1. opsonize cells or activate complement
2. antibodies recruit neut and macs 3. bind to normal cell receptors and interfere with functioning |
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Type II HS test
|
direct and indirect Coombs
|
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Type III HS
|
Immune complex
antigen-antibody-complement |
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Type III HS mechanism
|
IgG complexes activate complement
this attracts neuts, release lysosomal enzymes |
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Serum sickness
|
type III HS
antibodies to foreign proteins are produced takes 5 days immune complexes deposit in membranes there they fix complement this causes tissue damage *more common than Arthus reaction* |
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Symptoms of serum sickness
|
fever
urticaria arthralgias proteinuria lymphadenopathy 5-10 days after exposure *usually caused by drugs* |
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Arthus reaction
|
type III HS
local subacute intradermal injection induces antibodies form complexes in skin |
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Arthus reaction symptoms
|
edema
necrosis |
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Type III HS test
|
immunofluourescent staining
|
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Type IV HS
|
Delayed
T cell mediated not transferable by serum 4 Ts: T cells, Transplant rejections, TB skin test, Touching (contact dermatitis) |
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Type IV HS mechanism
|
sensitized T enounter antigen and release lymphokines
this activates macs |
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Hypersensitivity reactions
ACID |
Anaphylactic and Atopic activation (I)
Cytotoxic (II) Immune complex (III) Delayed (IV) |
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Type IV HS test
|
PPD
(patch test) |
|
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Anaphylaxis (bee sting) HS?
|
I
|
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Allergic rhinitis HS?
|
I
|
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Hemolytic anemia HS?
|
II
|
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SLE HS?
|
III
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Poststreptococcal glom HS?
|
III
|
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Rheumatic fever HS?
|
II
|
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Goodpastures HS?
|
II
|
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Rheumatoid arthritis HS?
|
III
|
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Polyarteritis nodosa HS?
|
III
|
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Myasthenia gravis HS?
|
II
|
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Hypersensitivity pneumonitis (farmers lung) HS?
|
III
|
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Pemphigus vulgaris HS?
|
II
|
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Pernicious anemia HS?
|
II
|
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Idiopathic Thrombocytopenia purpura HS?
|
II
|
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Erythroblastosis fetalis HS?
|
II
|
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Bullous pemphigoid HS?
|
II
|
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Type 1 DM HS?
|
IV
|
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MS HS?
|
IV
|
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Guillain Barre HS?
|
IV
|
|
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Hashimotos thyroiditis HS?
|
IV
|
|
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Graft vs Host HS?
|
IV
|
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PPD HS?
|
IV
|
|
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Contact dermatitis HS?
|
IV
|
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|
Brutons agammaglobulinemia
|
dec production of B cells:
X linked recessive low levels of all classes recurrent bacterial infections after 6 mo normal pro-B Boys |
|
|
Thymic aplasia (DiGeorge)
|
dec production of T cells
Thymus and parathyroids fail to dev (failure of 3rd and 4th pharyngeal pouches) Tetany due to hypocalcemia recurrent viral and fungal infections heart defects 22q11 deletion |
|
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SCID
|
defect in B and T cells
due to defect in early stem cell different. recurrent viral, bact, fungal, prot infections no rejection of allografts (causes: no MHC II, no IL-12 receptors, adenosine deaminase def) |
|
|
IL-12 receptor deficiency
|
dec activation of T cells
disseminated mycobacterial infections due to decreased Th1 response |
|
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hyper IgM syndrome
|
Defect in CD40 ligand on Th cells
leads to inability to class switch severe pyogenic infections high IgM low everything else |
|
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Wiskott Aldrich syndrome
|
X linked defect in IgM response to polysaccharide capsules of bacteria.
high IgE and IgA low IgM pyogenic inf, thrombocytopenic purpura eczema |
|
|
Jobs syndrome
|
failure of IFN gamma production by Th
neutrophils fail to respond coarse facies, cold staph abscesses, retained primary teeth, high IgE Derm probs |
|
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Leukocyte adhesion deficiency
|
Defect in LFA-1 integrin (CD18)
recurrent bacterial inf absent pus neutrophilia delayed sep of umbilicus (probs phagocytosing) |
|
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Chediak Higashi syndrome
|
autosomal recessive
defect in microtubular formation defect in lysosomal emptying recurrent pyogenic inf by staph and strep partial albinism peripheral neuropathy |
|
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Chronic granulomatous disease
|
defect in microbicidal activity of neuts
lack of NADPH oxidase susc to opportunistic infections Staph, E coli, aspergillus |
|
|
Chronic mucocutaneous candidiasis
|
T cell dysfunction against candida
skin and mucous inf |
|
|
Selective immunoglobulin deficiency
|
usually IgA
defect in isotype switching sinus and lung infections milk allergies diarrhea anaphylaxis w/blood products w/IgA |
|
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Ataxia telangiectasia
|
defect in DNA repair enzyme w/IgA def
cerebellar probs (ataxia) spider angiomas (telangiectasia) |
|
|
IL-12 receptor deficiency
|
dec activation of T cells
disseminated mycobacterial infections due to decreased Th1 response |
|
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hyper IgM syndrome
|
Defect in CD40 ligand on Th cells
leads to inability to class switch severe pyogenic infections high IgM low everything else |
|
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Wiskott Aldrich syndrome
|
X linked defect in IgM response to polysaccharide capsules of bacteria.
high IgE and IgA low IgM pyogenic inf, thrombocytopenic purpura eczema |
|
|
Jobs syndrome
|
failure of IFN gamma production by Th
neutrophils fail to respond coarse facies, cold staph abscesses, retained primary teeth, high IgE Derm probs |
|
|
Leukocyte adhesion deficiency
|
Defect in LFA-1 integrin (CD18)
recurrent bacterial inf absent pus neutrophilia delayed sep of umbilicus (probs phagocytosing) |
|
|
Chediak Higashi syndrome
|
autosomal recessive
defect in microtubular formation defect in lysosomal emptying recurrent pyogenic inf by staph and strep partial albinism peripheral neuropathy |
|
|
Chronic granulomatous disease
|
defect in microbicidal activity of neuts
lack of NADPH oxidase susc to opportunistic infections Staph, E coli, aspergillus |
|
|
Chronic mucocutaneous candidiasis
|
T cell dysfunction against candida
skin and mucous inf |
|
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Selective immunoglobulin deficiency
|
usually IgA
defect in isotype switching sinus and lung infections milk allergies diarrhea anaphylaxis w/blood products w/IgA |
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Ataxia telangiectasia
|
defect in DNA repair enzyme w/IgA def
cerebellar probs (ataxia) spider angiomas (telangiectasia) |
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|
CVID
|
normal number B cells
dec plasma cells defect in B cell maturation dec Ig 20s to 30s risk of autoimmune dis and lymphoma |
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ANA
|
SLE
|
|
|
Anti-dsDNA
anti-Smith |
Specific for SLE
|
|
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Antihistone
|
drug induced lupus
|
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|
anti-IgG (rheumatoid factor)
|
Rheumatoid arthritis
|
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|
Anticentromere
|
Scleroderma (CREST)
|
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Anti-Scl-70
|
Scleroderma, diffuse
|
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|
Antimitochondrial
|
Primary biliary cirrhosis
|
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|
Antigliadin
antiendomysial |
Celiac
|
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Anti-BM
|
Goodpastures
|
|
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Anti-desmoglein
|
Pemphigus vulgaris
|
|
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Antimicrosomal
antithyroglobulin |
Hashimotos
|
|
|
Anti-Jo-1
|
Polymyositis
dermatomyositis |
|
|
Angi-SS-A (anti-Ro)
|
Sjogrens
|
|
|
Anti-SS-B (anti-La)
|
Sjogrens
|
|
|
Anti-U1-RNP
|
Mixed connective tissue disease
|
|
|
Anti-smooth muscle
|
autoimmune hepatitis
|
|
|
Anti-glutamate decarboxylase
|
Type 1 DM
|
|
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cANCA
|
Wegeners
|
|
|
pANCA
|
other vasculitis
|
|
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HLA A3
|
Hemochromatosis
|
|
|
HLA B27
PAIR |
Psoriasis
Ankylosing Spondylitis IBS Reiters syndrome |
|
|
HLA B8
|
Graves
|
|
|
HLA DR2
|
MS
Hay fever SLE Goodpastures |
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|
HLA DR3
|
DM type 1
|
|
|
HLA DR4
|
Rheum arth
DM type 1 |
|
|
HLA DR5
|
Pernicious anemia- B12 def, Hashimotos
|
|
|
HLA DR7
|
Steroid responsive nephrotic syndrome
|
|
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Autograft
|
from self
|
|
|
allograft
|
from nonidentical individual
same species |
|
|
syngeneic graft
|
identical twin or clone
|
|
|
xenograft
|
diff species
|
|
|
hyperacute rejection
|
antibody mediated
preformed antidonor abs in transplant recipient (ABs FROM HOST) minutes |
|
|
acute rejection
|
cell mediated
host Tc react against foreign MHC T CELLS FROM HOST weeks |
|
|
chronic rejection
|
T cell and antibody mediated
vascular damage (obliterative vascular fibrosis) irreversible months to years host T cells see donor MHC I as self MCH I presenting foreign antigen (HOST T CELLS) |
|
|
graft vs. host disease
|
maculopapular rash
jaundice hepatosplenomegaly diarrhea T CELLS FROM GRAFT ATTACK HOST |
