Immunology Flashcards
1
Q
- Pattern Recognizing Proteins?
- PAMP?
- Toll like receptors?
- DAMP?
- TLR4? TLR2? TLR3?
- Cytokine?
- Chemokine?
- Immature DC’s are great at? Activated via?
- Mature DC does what?
A
- Proteins on a cell expressed by cell to identify PAMPs
- Foreign molecule structure on pathogens
- Type of PRP
- Stress or damage indicators for inflammation
- Endotoxin lipopollysac. (gram - bacteria); Peptidoglycan (gram - bacteria) dsRNA (virus)
- Protein for WBC’s to move toward
- Protein that attracts other cells
- Phagocytes; cyto/chemokines
- Presents antigen
2
Q
- Stem cell: Give rise to?
- B Cell: Part of this response? Produce? Become?
- T Cells: Mature where? Type of immunity?
- Pre T Cell made where? Markers?
- Self tolerance?
- Lymph nodes: Percent exported here?
- What is Bursa of Fabricius?
- Pro B Cells: Called? Begin to make? Only? Chances?
- Pre B Cells: Have what? Chain? Either? Chances?
- Immature B Cells: Has surface? Decides?
- Mature B Cell has?
A
- Stem and daughter
- Humoral; Ab; memory cells
- Thymus; cell mediated
- Bone marrow; none
- No immune response
- 1%
- B Cell precursors from bone marrow finishes development here in birds
- Proginitors; cytoplasmic mu heavy chains; M or P 2
- Cytoplasmic mu chains light; M or P, K or L; 4
- Surface IgM to show world; clonal abortion stage
- Both IgM and IgD
3
Q
- Antibody response: Comes first? Next? Memory cells are?
- Made by fetus? Actively transported across in big doses before pregnancy? In milk? IgG half life? Make IgA when? Make IgG when?
- New born titer: If IgM? If IgG?
- Elderly restore T cells until when? Great with what type of antigens? Not great with what? Ex?
A
- IgM; IgG; IgG
- IgM; IgG; IgA; 3 weeks; 3 months; 3-6 weeks
- Came from baby = bad
- Came from mom = good
- 40; similar to youth; new ones; SARS
4
Q
Antibodies:
- Structure? (6)
- H chain types?
- Light chain types?
- CDR’s?
- IgG structure? IgA? IgD? IgE? IgM? Size order?
- Combining site?
- Allotype?
- Subclass?
- Idiotype?
- Valence?
- PPT?
- Agglunation?
- Epitopes?
A
- FAB = VL, CL, VH, CH1; Fc = CH2, CH3 X 2
- A, E, D, G, M
- K or L (same on both sides)
- Complementary binding region; 3 hypervariable domains make this up
- G, E, D: 2 L, 2 G/E/D chains: A: 4 Light, 4A, 1 Joining, 1 Secretory: M = 10 light, 10 mu, 1 joining
M>A>E>D>G - VL + VH
- slightly different sequences in HC region
- Minor allelic differences b/n patients
- CDR AA sequence in combining region
- # of determinants an Ab can bind (at least 2)
- Large complexes form this
- Big complexes fall out of solution
- AA’s on antigen that Ab interacts with
5
Q
Antibodies:
- IgG: Abundance? Placenta? 1/2 life? Compliment?
- IgM: Shows up? Valence? Complement?
- IgA: Found where? Protected from digestion?
- IgD: Function?
- IgE: Adheres to? Triggers? Important for?
- Best ppt formed with?
- Innate complement pathways?
- Classic pathway?
- Alternative pathway?
- Lectin pathway?
- Opsonizing?
- Lytic?
- Anapholaxic?
- Chemotactic?
A
- most abundant; only that crosses; 3 weeks; takes 2 IgG’s close together
- First; decavalent; best b/c it can bind 2 to same Ab
- Mucus membranes; secretory element
- B cell receptor
- Mast/B cells; histamine release; signaling eisono.
- 1/2 Ab and 1/2 Antigen
- Lectin and Alternative
- IgG and IgM: 2 FC’s activate C1Q-4-2-3-5…9
- IgA activated: 3-5-6….9
- Mannose binding protein - 4-2-3-5….9
- C3B adheres to membrane to attract macs
- MAC C5-9 form lesion
- C3A, C4A, C5A release histamine from mast cells
- C5A chemotaxic for neutrophils
6
Q
- Cross reactivity: Good Ex? Bad Ex?
- Instructional theory?
- Clonal selection?
- Allotypes?
- Primary transcript made of? Then?
- Class switching? Can only move? Can only change? Not?
- 4 steps to increase Ab diversity?
- V(D)J: Why is (D)
- Somatic mutation: Passed on to children? How?
A
- One Ab reacts with >1 antigen; Cowpox and small pox; Ab triggered then attacks heart
- Abs conform to antigen
- Cell makes Abs and not dependent on outside world
- Lambda/Kappa L chain on diff. chrom.
- VDJC M,D; delta or mu are spiced off
- Start as IgM or IgD but can then switch, down stream (m,d,g,e,a); heavy chain C region, not light chain or variable
1. ) 2000 genes (1k L, 1000 H)
2. ) VDJ joining
3. ) TdT adds/takes away
4. ) VDJ hypermutable when dividing, C to U then removed and replaced - Variable light chains only have VJ
- Not passed on; TdT and end joining
7
Q
T Cells:
- TH1: Type? Release? Which attracts? These release? (2)
- TH17: Make? Which attracts? Type? Implicated in?
- TH2: Circulate? Secrete? (2) Attracts? Leads to? Gives rise to? Suppresses?
- TfH: Some migrate to? Redirect B cells?
- Treg: Suppress? Make? (2)
- CTL: Help cells apoptose via? (2)
- 4 markers and on what cells?
- Lymphokine?
- Chemokine?
- Cytokine?
- Mitogen? Specific? Binds? Not?
A
- Proinflammatory; INFgamma; monocytes/macs (angry); TNFa and IL which increase inflammation
- Proinflamm.; IL17; even angrier macs; auotiumm
- Blood to find antigen; IL4 = chemotactic for eisono/suppress THI differ.; IL13 = M2 macs for healing; TH2 follciular cells push B cells to IgE
- Cortex to help B cells; direct B cells to IgG,IgE, IgA
- Other T cells; IGFbeta, IL10
- 1.) Activate FAS (CD95) 2.) Secrete lytic granules
- CD3 = All T cells; CD4= Th; CD8= CTL; CD20= B
- Short range mediator made by lymphocytes
- Signal by any cell that increase imflammation
- Mediator by any cell that effects same or different cell type
- Protein that stimulates T Cell division; no; CD3 ; binding site
8
Q
- T Cell Receptors: Only see antigens via? Focus on? Structure?
- Activation? (2 steps?)
- TH cascade? (4)
- CTL cascade? (4)
- MHC 1?
- MHC 2?
- T dependent antigens?
- T independent antigens? Often happens with? Not great with?
- TfH and B cells cascade? (4)
- Why is second exposure faster?
A
- MHC; Cells surfaces not free antigen; a and B chain with 2 CDR’s x 2
- 1.) Antigen with MHC presented 2.) 2nd signal from APC (IL12)
- Antigen enters, Ingested by DC, Peptides placed on Class 2 MHC, TH recognizes
- Protein made in cell, chopped to peptides, placed on class 1 MHC, CTL recognizes
- On all nucleated cells
- On DC’s, macs, B Cells
- Exposed to antigen and multiple Abs produced
- Don’t need T cells; carbs; peptide antigens
- B cell binds epitope, endocytosed, peptide to MHC 2, TfH recognizes diff. epitope, releases helper lymphokines
- 1st time DC’s must bring antigen; second time circulating t cells recognize antigen and respond
9
Q
- Transplant:
- Histocompatibility in humans? A/B? D(P,Q,R)? Located on what gene?
- Alloantigen?
- Haplotype?
- Best donors: Must match? Why? Who is best match? Then? Parents?
- Bone marrow transplant?
- What is perfect match?
- One way mixed leukocyte test? (3 steps)
- Rejection pathway: Foreign mac with TH? Leads to release of? (2) CTL with any foreign cell?
- HLA-DR3/4 related to?
- How do T cells recognize foreign MHC?
A
- HLA: Class 1 MHC all nucleated cells; Class 2 MHC B,Mac, DC; short arm Chrom. 6
- Antigen that is part of self recognition system
- Combo of alleles that are transmitted together; codominate presentation (1 from mom/dad)
- HLA-DR; signals both responses; Identical twin; sibling (25%); only half similar
- Should be higher match
- 10/10 A,B,C, DR, DQ
- T cells of donar are killed, Cells of both are mixed, check how many divisions occur
- IL12 from foreign mac stimulates TH; IFNgamma (increased inflammation); IL2 (activates CTL)
- Juvenile diabetes
- Squeeze to fit in their MHC
