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138 Cards in this Set
- Front
- Back
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in the lymph node, where are B cells?
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follicle (outer cortex)- primary are dense and dormant, secondary have pale centers and are active
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where are the T-cells in the lymph node?
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paracortex- between follicles and medulla. Contains high endothelial venules through which B and T cells enter from blood.
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what structure in the lymph node has extreme enlargement in an extreme cellular immune response?
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paracortex (tcells)
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lymph drainage: stomach
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celiac
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lymph drainage: duodenum and jejunum
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superior mesenteric
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lymph drainage: sigmoid colon
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colic-->inferior mesenteric
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lymph drainage: rectum and anal canal above pectinate
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internal iliac
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lymph drainage: anal canal below pectinate
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superficial inguinal
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lymph drainage: testes
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superficial and deep plexuses-- para-aortic
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lymph drainage: scrotum
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superficial inguinal
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lymph drainage: thigh (superficial)
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superficial inguinal
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lymph drainage: lateral side of dorsum of foot
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popliteal
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lymph drainage: right arm and right half of head
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right lymphatic duct (everything else goes through lymphatic duct)
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where are T-cells found in the spleen?
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PALS periarterial lymphatic sheath and red pulp.
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where are B cells found in the spleen?
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follicles within the white pulp of the spleen
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embryonic origin of Thymus:
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3rd branchial pouches.- lymphocytes of mesenchymal origin.
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briefly describe differentiation of T cells
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T-cell precursor (bone marrow) --> CD4/8 + to CD4 and CD8+ (thymus)--> CD8 to cytotoxic Tcell (lymph) and CD4 to Th1 (IL-2, INF-g) and Th2 (IL-4/5)
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what Interleukens help differentiate Th1 and Th2?
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IL-12 to Th1, IL-4 to Th2 (remember it also makes IL-4)
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what are the MHC I HLA genes
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HLA-A, HLA-B, HLA-C - expressed on most nucleated cells- mediates viral immunity
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what are the MHC II HLA genes
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HLA-DR, HLA-DP, HLA-DQ- only on antigen presenting cells
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what is responsible for hyperacute organ rejection
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antibodies
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what is resonsible for allograft rejection (acute and chronic)
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T-cells
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what do CD-4 and CD-8 bind to?
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CD-8 binds to MHC I (cytotoxic T cells) CD-4 binds to MHC II (helper T cells)
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What are the 2 signals needed in T cell (helper) activation
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1) foreign molecule on MHC-II recognized by TCR, 2) costimulatory signal B7 (APC) ad CD28 (Tcell)
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what signals are needed for T cell (cytotoxic ( activation?
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1) endogenous proteins synthesized on MHC-I recognized by TCR, 2) IL-2 activation from Th cells.
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define Ig allotypes, isotypes and idiotypes:
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allo- polymorphism, iso - IgG, IgA etc, idio- Ig epitope determined by antigen binding site.
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who makes and what is the function of: IL-1
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Macs make- acute inflammation, induces chemokine production to recruit leukocytes, activates endotheliam to express adhesion molecules and is and endogenous pyrogen. Fever
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who makes and what is the function of: IL-2
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Th cells- stimulates T cell growth (Th and Tc)
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who makes and what is the function of: IL-4
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Th2 cells- promotes growth of B-cells and enhances class switching IgM to IgG
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who makes and what is the function of: IL-5
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Th2 cells- promotes differentiation of B-cells and enhances class switching to IgA- stimulates eosinophils
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who makes and what is the function of: IL-8
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Macs make, Major chemotactic factor for neutrophils (clean up on aisle 8)
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who makes and what is the function of: IL-10
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regulatory T cells- inhibits actions of activated T cells
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who makes and what is the function of: IL-12
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B cells and Macs- activates NK anf Th1 cells
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who makes and what is the function of: gamma- interferon
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Th1 cells- stimulates macs
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who makes and what is the function of: TNF
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macs- mediates septic shock- causes leukocyte recruitment, vascular leak.
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what cell: CD4, 3, 28, 40L
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T helper
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what cell: CD8, CD3, TCR
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T cytotoxic
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What cell: B7, CD19, CD20, CD21, CD40, MHCII
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B-cell
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What cell: MHCII, B7, CD40, CD14 Rc and C3b receptors
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Macrophage
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What cell: receptors for MHC I, CD16, CD56
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NK cells
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how is the membrane attack complex activated by classic and alternate pathway:
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classic: IgG and IgM; alternate: microbe molecules (esp LPS endotoxin)
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what are the primary bacterial opsonins
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C3b and IgG are the 2 primary ones
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complement system defect resulting in hereditary angioedema:
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C1 esterase inhibitor
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complement defect resulting in severe, recurrent pyogenic sinus and respiratory tract infections:
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C3b and IgG are the 2 primary ones
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complement defect resulting in neisseria bacteremia:
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C6-C8
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defect in DAF (decay accelerating factor) that help prevents compliment activation on self cells results in what disease?
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self-mediated lysis of RBCs- paroxysmal nocternal hemoglobinuria
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how do inferons alpha and beta work in innate immunity?
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inhibit viral protein synthesis- ribonuclease
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how does interferon gamma work in innate immunity?
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increase MHC I and II expression and antigen presentation in all cells
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arthus reaction takes place where?
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skin- type III reaction to intradermal injection of antigen.- edema, necrosis and activation of complement
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findings in serum sickness:
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fever, uritcatia, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure
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type I hypersensitivity mediated by what cells?
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mast and basophils release vasoactive amines (Fc receptor especially to IgE). Worse after preformed anitbodies
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4 Ts of type IV mediated hypersensitivity:
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T cells, transplant rejection, TB skin tes, Touching (contact dermatitis) - t cells release lymphokines (activates macs)
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type of hypersensitivity reaction: allergic rhinitis
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Type I
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type of hypersensitivity reaction: hemolytic anemia
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Type II
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type of hypersensitivity reaction: idiopathic thrombocytopenic purpura
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Type II
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type of hypersensitivity reaction: erythroblastosis fetalis
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Type II
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type of hypersensitivity reaction: rheumatic fever
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Type II
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type of hypersensitivity reaction: goodpasture's
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Type II
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type of hypersensitivity reaction: bullous pemphigoid
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Type II
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type of hypersensitivity reaction: graves disease
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Type II
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type of hypersensitivity reaction: SLE
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Type III
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type of hypersensitivity reaction: Rheumatoid arthritis
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Type III
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type of hypersensitivity reaction: polyarteritis nodosum
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Type III
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type of hypersensitivity reaction: poststreptococcal glomerulonephritis
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Type III
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type of hypersensitivity reaction: serum sickness
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Type III
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type of hypersensitivity reaction: arthus reaction
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Type III
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type of hypersensitivity reaction: hypersensitivity pneumonitis
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Type III
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type of hypersensitivity reaction: DM type 1
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Type IV
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type of hypersensitivity reaction: MS
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Type IV
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type of hypersensitivity reaction: Guillain-Barre
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Type IV
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type of hypersensitivity reaction: hashimoto's thyroiditis
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Type IV
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type of hypersensitivity reaction: graft-versus-host disease
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Type IV
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type of hypersensitivity reaction: PPD
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Type IV
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type of hypersensitivity reaction: contact dermatitis
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Type IV
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12 month old boy with recurrent bacterial infections after 6 months age. Decrease # Bcells
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Bruton's agammaglobinemia- X-linked recessive defect in tyrosine kinase- low level of all classes of Igs.
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Tetany and recurrent viral and fungal infections. Congenital defect in heart and great vessels.
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Thymic aplasia (DiGeorge syndrom)- 22q11
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embryonic origin of thymus and parathyroid
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3rd and 4th pharyngeal pouches (digeorge)
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recurrent viral, bacterial, fungal, protozoal infection.
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SCID- defect in early stem cell differentiation- multiple causes (MHC II antigens, IL-2 receptors, Adenosine deaminase deficiency)
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disseminated mycobacterial infections
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IL-12 receptor deficiency- decrease Th1 response.
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early severe pyogenic infections - high IgM, low IgG, A, E.
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hyper IgM syndrome- defect in CD40 ligand on CD4 helper cells - help class switch.
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recurrent pyogenic infections, thrombocytopenic purpura, eczema
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Wiskott-Aldrich syndrom- X-linked defect in mounting IgM respnse to capsular bacteria. High IgA levels, low IgM.
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coarse facies, cold staph abscesses, retained primary teeth, increase IgE, dermatologic problems.
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Job's syndrome- failure of IFN-g production by helper T cells leading to no neutrophil response.
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recurrent bacterial infections, absent pus formation, delayed seperation of umbilicus.
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LAD- leukocyte adhesion deficiency syndrom (type I)- defect in LFA-1 integrin proteins on phagocytes.
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recurrent pyogeneic infections by staph and strep, partial albinism, peripheral neuropathy.
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chediak-higashi- AR- microtubular defect and lysosomal emptying of phagocytic celss.
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susceptability to opportunistic infections with bacteria, especially Staph, E.coli, aspergillus. Negative nitroblue tetrazolium test.
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CGD- lack of NADPH oxidase acitvity or similar enzymes.
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skin and mucous membrane candida infections-
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chronic mucocutaneous candidiasis- t cell dysfunction against candidiasis albicans specifically
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sinus and lung infections, milk allergies and diarrhea
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IgA deficiency (most common selective deficiency)
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cerebellar problems (ataxia) and spider angiomas (telangectasias). Decrease IgA.
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ataxia-telangectasia- defect in DNA repair -
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normal B cell number, decrease plasma cells and Ig
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common variable immunodeficiency- defect in B-cell maturation- can be acquired (20-30s)
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associated disorder: antinuclear antibodies ANA
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SLE
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associated disorder: anti-dsDNA and Smith
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specific for SLE
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associated disorder: antihistone
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drug induced Lupus
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associated disorder:anti-IgG
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Reumatoid arthritis
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associated disorder: anticentromere
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scleroderma (crest)
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associated disorder: antiScl-70
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scleroderma (diffuse)
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associated disorder: antimitochondrial
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primary biliary cirrhosis
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associated disorder: antigliadin
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celiac disease
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associated disorder: antibasement membrane
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goodpasture's
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associated disorder: anti-epithelial cell
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pemphigus vulgaris
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associated disorder: antimicrosomial, anti-thyroglobulin
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Hashimoto's
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associated disorder: anti-Jo-1
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polymyositis, dermatomyositis
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associated disorder: anti-SS-A (anti Ro)
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sjogren's
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associated disorder: anti-SS-B (anti La)
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sjogren's
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associated disorder: anti-U1RNP
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mixed connective tissue disease (ribonucleoprotein)
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associated disorder: anti-smooth muscle
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autoimmune hepatitis
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associated disorder: anti-glutamate decarboxylase
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DM type1
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associated disorder: anti-cANCA
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wegener's granulomatosis
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associated disorder: anti-pANCA
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microscopic polyangiitis, churg-strauss
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associated disorders: HLA-B27
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PAIR- psoriasis, ankylosing spondylitis, inflammatory bowel disease, Reiter's syndrom
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associated disorders: HLA-B8
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grave's and celiac sprue
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associated disorder: HLA-DR2
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MS, hay fever, SLE, goodpastures
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associated disorders: HLA-DR3
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DM type1
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associated disorders: HLA-DR4
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Rheumatoid arthritis, DM type 1
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associated disorders: HLA-DR-5
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Pernicious anemia, hashimoto's
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associated disorder: HLA-DR7
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steroid responsive nephrotic syndrome
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immunosupressants that are nephrotoxic:
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cyclosporine (mannitol diuresis helps), Tacrolimus
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MOA of cyclosporine
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binds cyclophilins and blocks the diff and activation of T cells by inhibiting calcineurin- prevents production of IL-2 and receptor.
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MOA of tacrolimus
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similar to cyclosporin- binds FK-binding protein, inhibiting secretion of IL02 and other cytokines.
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Tacrolimus toxicity
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nephrotoxic, peripheral neuropathy, HTN, pleural effusion, hyperglycemia
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MOA of Azothioprine
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antimetabolite precursor of 6 mercaptopurine that interferes with metabolism and synthesis of nucleic acids (toxic to lymphocytes)
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AE's for azothioprine
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Bone marrow suppresion. Increase toxic effects by allopurinol because active metabolite is metabolized by xanthine oxidase
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uses for azothuoprine
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kidney transplant, autoimmune glomerulonephritis and hemolytic anemia
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MOA muomonab CD3 (OKT3)
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Mab binds CD3 on surface T cells and blocks tcell signal transduction. (kidney transplant)
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muromonab (OKT3) AE's
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cytokine release syndrome, hypersensitivity reaction
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MOA sirolimus, AE's
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binds to mTOR- inhibits Tcell proliferation in response to IL-2; Aes- hyperlipidemia, thrombocytopenia, leukopenia
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MOA mycophenolate mofetil
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inhibits de-novo guanine synthesis and blocks lymphocyte proliferation
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MOA daclizimab
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Mab for IL-2 receptor on activated Tcells
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clinical use(s) of recombinant: IL-2
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renal cell carcinoma, metastatic melanoma
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clinical use(s) of recombinant: erythropoietin
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anemias (esp in renal failure)
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clinical use(s) of recombinant: (GCSF)
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recovery of bone marrow
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clinical use(s) of recombinant: GMCSF
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recovery of bone marrow
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clinical use(s) of recombinant: alpha- interpheron
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Hepatitis B and K, Kaposi's sarcoma, leukemias, malignant melanoma
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clinical use(s) of recombinant: beta-interpheron
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MS
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clinical use(s) of recombinant: gamma-interpheron
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CGD
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clinical use(s) of recombinant: IL-11
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thrombocytopenia
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what type of rejection: irreversible ab-mediated vascular damage (fibrinoid necrosis)
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chronic rejection
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rejection type: cell mediated (cytotoxic Tcells) agains forein MHCs. Weeks after transplantation, reversible
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acute rejection
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rejection type: preformed antidonor abs
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hyperacute- within minutes
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