immune_receptors

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Author:
soren101
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30193
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immune_receptors
Updated:
2010-08-22 12:28:54
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immunology receptors ms1
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Description:
immune receptors and genetic diversity
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  1. WHAT 2 FORMS OF ANTIBODY ARE MADE BY B CELLS AND WHAT ARE THEIR
    RESPECTIVE FUNCTIONS?
    SECRETED EFFECTOR MOLECULES AND MEMBRANE BOUND RECEPTORS
  2. WHAT IS THE BASIC STRUCTURE OF AN ANTIBODY MOLECULE?
    COMPOSED OF 4 POLYPEPTIDE CHAINS JOINED BY DISULFIDE BONDS

    2 IDENTICAL PAIRS OF HEAVY AND LIGHT CHAINS
  3. HOW MANY CLASSES OF ANTIBODY ARE PRESENT IN HUMANS AND HOW ARE THE
    DIFFERENT CLASSES DISTINGUISHED FROM ONE ANOTHER?
    IgM – FIRST PRODUCED BY MATURE B-CELLS

    IgD

    IgG

    IgE

    IgA
  4. WHAT IS MEANT BY THE VARIABLE DOMAIN OF THE HEAVY AND LIGHT CHAINS OF
    ANTIBODY?
    FIRST 110 AMINO ACIDS IN AMINO TERMINAL SEQUENCE

    INVOLVED IN ANTIGEN BINDING
  5. HOW MANY MOLECULES OF ANTIGEN CAN ONE Fab FRAGMENT BIND?
    1
  6. WHAT PORTION OF THE ANTIBODY MOLECULE CONSTITUTES THE Fc FRAGMENT?
    2 HEAVY CHAIN FRAGMENTS

    NO ANTIGEN BINDING ACTIVITY
  7. HOW DOES THE HINGE REGION AFFECT THE FUNCTION OF ANTIBODY?
    FLEXIBILITY BETWEEN Fab AND Fc

    PROLINE RICH

    PROTEASE SINSITIVE

    MOST INTER-CHAIN DISULFIDES ARE FOUND HERE

    DETERMINES AVAILABILITY FOR ANTIGEN BINDING BASED ON STERIC CONSIDERATIONS
  8. WHAT IS THE MAIN STRUCTURAL FEATURE OF Ig DOMAINS AND HOW IS THIS
    STRUCTURE FORMED IN 3-D SPACE?
    4 OR 5 SIMILAR DOMAINS OF 110 AMINO ACIDS EACH

    EACH DOMAIN CONTAINS ONE INTRA-CHAIN DISULFIDE LINKAGE THAT IS IMPORTANT FOR TERTIARY STRUCTURE
  9. DEFINE CDRs AND EXPLAIN HOW THEY CONTRIBUTE TO ANTIGEN-ANTIBODY
    INTERACTIONS?
    COMPEMENTARITY DETERMINING REGIONS

    SPECIFIC REGIONS THAT SHOW STRUCTURAL VARIABILITY KNOWN AS HYPERVARIABLE REGIONS

    3 CDRs FOR EACH HEAVY AND LIGHT CHAIN, 6 ON EACH ARM; 12 TOTAL

    LINE THE SHALLOW GROVE FORMED BY THE APPOSITION OF THE 3-STRANDED B-SHEETS MAKE UP THE HEAVY/LIGHT CHAINS THAT FORM ANTIGEN BINDING SITE
  10. COMPARE/CONTRAST THE TERMS AFFINITY AND AVIDITY AS THEY PERTAIN TO
    ANTIBODY-ANTIGEN INTERACTIONS
    AFFINITY IS A THERMODYNAMIC VALUE THAT QUANTIFIES THE STRENGTH OF ANTIBODY BINDING TO AN ANTIGENIC DETERMINANT

    AVIDITY IS THE OVERALL INTERACTION STRENGTH OF 2 OR MORE ANTIBODIES BINDING TO ANTIGENS AND IS OFTEN GREATER THAN SUM OF INDIVIDUAL ANTIBODY AFFINITY
  11. PRO-B CELLS
    EARLIEST STAGE OF B-CELL DIFFERENTIATION

    LYMPHOID PROGENITORS

    ANTIGEN-INDEPENDENT
  12. PRE-B CELLS
    FROM PRO-B CELLS

    FIRST TO EXPRESS Ig HEAVY CHAIN IN CYTOPLASM

    M-HEAVY CHAIN IS SYNTHESIZED FIRST BEFORE LIGHT CHAIN

    ANTIGEN INDEPENDENT
  13. IMMATURE IgM+B CELLS
    FROM PRE-B CELLS

    LIGHT CHAIN SYNTHESIS AND ASSEMBLY WITH HEAVY CHAINS FORMING COMPLETE IgM ANITBODY MOLECULE THAT IS EXPRESSED ON CELL SURFACE

    ANTIGEN INDEPENDENT
  14. MATURE-B CELLS
    FROM IMMATURE-B CELLS

    B CELL BEGINS TO EXPRESS BOTH IgM AND IgD ON SURFACE, EACH EXPRESSING THE EXACT SAME VARIABLE REGION AND THUS SAME SPECIFICITY FOR ANTIGEN

    MONOSPECIFIC
  15. ANTIGEN-DEPENDENT B-CELL DIFFERENTIATION
    MATURE B-CELLS ACTIVATED BY SPECIFIC ANTIGEN

    BEGIN TO SECRETE IgM

    HEAVY CHAIN CLASS SWITCHING, EXPRESSION OF OTHER ANTIBODIES

    PLASMA CELLS

    MEMORY CELLS
  16. PLASMA CELLS
    CONTAIN LOTS OF RER AND SECTRETE ANTIBODY AT VERY HIGH RATE/QUANTITY

    DON’T EXPRESS MEMBRANE FORM OF ANTIBODY

    END STAGE OF B-CELL DIFFERENTIATION

    ANTIGEN DEPENDENT
  17. MEMORY CELLS
    LONG-LIVING LYMPHOCYTES RESPONSIBLE FOR SECONDARY RESPONSE

    USUALLY EXPRESS ISOTYPES OTHER THAN IgM ON SURFACE

    ANTIGEN DEPENDENT
  18. AT WHAT STAGE OF B-CELL DEVELOPMENT IS THE ANTIBODY HEAVY CHAIN FIRST
    EXPRESSED?
    PRE-B CELLS

    PRO-B CELLS --> PRE-B CELLS
  19. WHAT IS THE END-STAGE CELL IN THE B-CELL DEVELOPMENT LINEAGE?
    PLASMA CELLS

    MEMORY CELLS?
  20. HOW CAN A FINITE GENOME ENCODE ANTIBODIES CAPABLE OF RECOGNIZING AN ALMOST
    INFINITE # OF ANTIGENS?
    VARIABLE REGIONS ENCODED BY MULTIPLE GENE SEGMENTS

    GENE REARRANGEMENT DURING ANTIGEN-INDEPENDENT PHASE
  21. WHAT ARE THE DIFFERENT GENE SEGMENTS THAT ENCODE Ig HEAVY CHAINS AND
    WHAT IS THEIR ORDER OF REARRANGEMENT DURING B-CELL DEVELOPMENT?
    4 GENE SEGMENTS ON CHROM 14 – V,D,J,C

    D --> J

    THEN V --> DJ TO FORM M-HEAVY-CHAIN GENE

    M-HEAVY-CHAIN GENE EXPRESSED FIRST AND MEMBRANE FORM ACTIVATE K-LIGHT-CHAIN REARRANGEMENT
  22. WHAT IS RELATIONSHIP BETWEEN EACH PROTEIN DOMAIN IN ANTIBODY HEAVY/LIGHT
    CHAINS AND THE EXONS IN THE HEAVY/LIGHT CHAIN GENES?
    EACH PROTEIN DOMAIN INCLUDING HINGE, TAILPIECE, TRANSMEMBRANE, AND CYTOPLASMIC IS ENCODED BY A SEPARATE EXON IN THE FUNCTIONALLY ASSEMBLED CHAIN
  23. WHY CAN A Vh GENE SEGMENT NOT JOIN DIRECTLY TO A Jh GENE SEGMENT DURING
    HEAVY CHAIN REARRANGEMENT?
    D --> J MUST BIND FIRST
  24. IF A PERSON LACKED RAG-1 AND/OR 2, WHAT AFFECT WOULD YOU EXPECT THIS
    DEFICIENCY TO HAVE ON THE IMMUNE SYSTEM AS A WHOLE AND THE GENERATION OF
    ANTIBODY DIVERSITY?
    UNABLE TO FORM MATURE-B CELLS OR T-CELLS

    NO ADAPTIVE IMMUNITY

    Decrease the overall diversity of antibodies because of the lack of the recombination mechanism
  25. WHAT 3 MECHANISMS CONTRIBUTE TO ANTIBODY DIVERSITY?
    Ig GENE REARRANGEMENT (V,D,J COMBOS)

    HEAVY/LIGHT CHAIN COMBOS

    JUNCTION DIVERSITY
  26. WHAT MECHANISMS ACCOUNT FOR GREATER DIVERSITY IN CDR3 THAN IN THE REST
    OF THE VARIABLE REGION?
    IMPRECISE JOINING OF V,D,&J SEGMENTS
  27. DESCRIBE ONE ADVANTAGE AND ONE DISADVANTAGE OF N AND P NUCLEOTIDE
    ADDITION DURING THE REARRANGEMENT OF ANTIBODY HEAVY CHAIN GENE SEGMENTS
    GREATER DIVERSITY

    BUT OFTEN LEAD NON-PRODUCTIVE REARRANGEMENTS DUE TO READING-FRAME SHIFTS
  28. WHAT MECHANISM ALLOWS B CELLs TO COEXPRESS IgM AND IgD?
    ALTERNATIVE RNA TERMINATION

    PROCESSING OF LONG RNA TRANSCRIPT

    IgM AND IgD DIFFERENTIALLY REGULATED DURING B-CELL MATURATION

    IgD LEVEL ON SURFACE OF IMMATURE B CELLS IS LOW OR ABSENT

    MATURE-B CELLS HAVE HIGHER DENSITY OF IgD RELATIVE TO IgM

    BOTH ARE EXPRESSED FROM SAME TRANSCRIPTION UNIT
  29. HOW DOES THE MEMBRANE ANTIBODY DIFFER FROM SECRETED FORM AND HOW DOES
    THE B CELL MAKE BOTH FORMS?
    MIg CONTAINS A HYDROPHOBIC TRANSMEMBRANE REGION AND A CYTOPLASMIC TAIL SEQUENCE AT THE CARBOXYL END

    SEPARATE EXONS ENCODE SECRETED OR MEMBRANE-BOUND ENDS

    REGULATED BY ALTERNATIVE RNA PROCESSING EVENTS INVOLVING CHOICE OF 2 DIFFERENT RNA

    CLEAVAGE AND POLY-A SITES
  30. WHAT IS ALLELIC EXCLUSION AND WHAT ASSURES THAT Ig GENES ARE ALLELICALLY EXCLUDED?
    EXPRESSION OF A GENE FROM ONLY ONE OF TWO PARENTAL CHROMS

    MUST FOLLOW SEQUENCE OF “IF/THEN” STEPS, i.e. IF FIRST CHROM MAKES NON-PRODUCTIVE PROTEIN THEN 2ND CHROM IS ACTIVATED.
  31. HOW IS T-CELL RECEPTOR DIVERSITY GENERATED?
    3 HIGHLY VARIABLE REGION DOMAINS THAT CORRESPOND TO THE CDRs FOUND IN Ig

    V, D, J, AND C REGION GENES SIMILAR TO Ig HEAVY CHAIN

    JUNCTIONAL DIVERSITY – CONTRIBUTES MORE TO TCR DIVERSITY THAN IN Ig. N & P NUCLEOTIDE ADDITION OCCURS BOTH IN ALPHA & BETA CHAINS, D REGIONS CAN OFTEN BE TRANSLATED IN ALL 3 READING FRAMES

    ASSOCIATION OF DIFFERENT ALPHA AND BETA CHAINS

    NO SIGNIFICANT SOMATIC MUTATION IN TCR GENES
  32. HOW DOES RECOGNITION OF ANTIGEN BY THE T CELL RECEPTOR DIFFER FROM RECOGNITION OF ANTIGEN BY THE B CELL RECEPTOR?
    T CELLS USUALLY ONLY RECOGNIZE PROTEIN ANTIGENS
  33. DESCRIBE THE ANTIGEN SPECIFIC RECEPTOR ON T CELLS – WHICH PART
    RECOGNIZES THE ANTIGEN?
    2 CLASSES OF TCRs (T-CELL RECEPTORS), ALPHA-BETA AND GAMMA-DELTAHETERODIMER

    SIMILAR TO Ig
  34. HOW ARE THE BCR AND TCR SIMILAR/DIFFERENT?
    BOTH ARE DISULFIDE LINKED WITH VARIABLE, CONSTANT, TRANSMEMBRANE AND CYTOPLAMIC REGIONS

    BCRs HAVE HEAVY/LIGHT CHAIN INTERACTIONS WHILE TCRs HAVE ALPHA-BETA ACIDIC-BASIC CHAIN INTERACTIONS

    TCRs ARE MEMBRANE-BOUND ONLY
  35. HOW DO ALPHA-BETA T CELLS DIFFER FROM GAMMA-DELTA TCELLS?
    ALPHA-BETA T CELLS ONLY RECOGNIZE ANTIGENS ASSOCIATED WITH MHC MOLECULES

    GAMMA-DELTA T CELL FUNCTION IS NOT KNOWN AND IS 10% OF MATURE PERIPHERAL T-CELL
  36. EXPRESSION OF THE TCR ON THE CELL SURFACE REQUIRES WHAT PROTEINS IN ADDITION TO THE AB/GD CHAINS?
    CD3 COMPLEX (CD GAMMA, DELTA, AND EPSILON)

    ZETA PROTEIN LOCATED ON THE CYTOPLASMIC SIDE

    SERVE TO TRANSMIT SIGNALS TO THE INTERIOR OF THE CELL ONCE THE TCR ENGAGES ANTIGEN
  37. DURING INTRACELLULAR INFECTION, WHAT 2 THINGS MUST HAPPEN FOR CTLs TO BE EFFECTIVE IN CELL MEDIATED IMMUNITY?
    1) CTL MUST BE ACTIVATED. ANTIGEN MUST BE PROCESSED BY PROTEOSOMES INTO SMALL FRAGMENTS AND PRESENTED TO CTLs BY APCs (DENDRIDIC, MACROPHAGES, B CELLS)

    2) ACTIVATED CTL MUST TARGET INFECTED HOST CELLS (AND DISREGARD NONINFECTED CELLS) BY REGOGNIZING BOTH THE ANTIGEN AND MHC I RECEPTORS
  38. DESCRIBE THE INTERACTION BETWEEN PROTEOSOMES, TAP, AND MHC I RECEPTORS
    DEGRADE INTRACELLULAR PROTEINS

    UPREGULATED BY CYTOKINES (IFN-GAMMA)

    PROTEINS TAGGED WITH UBIQUITIN ARE RAPIDLY DEGRADED AND PASSED INTO ER BY TAP 1&2

    MHC I RECEPTORS STICK TO TAB BY TAPSIN, WHERE THEY ARE PLACED INTO CLOSE PROXIMITY TO FRAGMENTS ENTERING THE ER
  39. DESCRIBE THE BASIC STRUCTURE OF MHC I RECEPTORS
    HEAVY CHAIN CONSISTINGOF 3 EXTRACELLULAR SEGMENTS (ALPHA 1,2&3), A MEMBRAIN SEGMENT, AND A CYTOPLASMIC SEGMENT

    BETA-2 MICROGLOBULIN NONCOVALENTLY ASSOCIATED WITH, AND NOT GENETICALLY ENCODED WITH, THE HEAVY CHAIN. MHC I CANNOT BE EXPRESSED WITHOUT B-2 MICROGLOBULIN

    NO RECOMBINATION AT THE DNA LEVEL

    ANTIGEN BINDS TO ALPHA 1&2 ON HEAVY CHAIN
  40. WHAT 2 CHARACTERISTICS PROVIDE MHC RECEPTORS WITH GENETIC DIVERSITYGIVEN GIVEN THAT THEY DO NOT UNDERGO RECOMBINATION?
    POLYGENIC, CONSISTING OF 3 ISOFORMS (A,B,&C) OF HEAVY CHAIN

    POLYMORPHIC, HUNDREDS OF ALLELES IN THE HUMAN POPULATION FOR THE 3 ISOFORMS A,B,&C.

    CO-DOMINANT EXPRESSION (ex. 2 FORMS OF B ISOFORM WILL BE EXPRESSED IF HETEROZYGOUS)
  41. HOW IS ANTIGEN REGOGNITION DIFFERENT BETWEEN B AND T CELLS?
    TCRs REQUIRE AN ADDITIONAL COMPLEX (CD3) FOR CELL ACTIVATION

    TCRs MUST ALSO HAVE DUAL RECOGNITION. THEY MUST BIND BOTH TO THE ANTIGEN AND TO THE ALPHA HELICAL COMPONENTS OF THE MHC RECEPTOR
  42. DESCRIBE T-CELL-ACTIVATION-SIGNALS 1 & 2
    SIGNAL 1 REQUIRES DUAL RECOGNITION BY TCRs OF BOTH ANTIGEN AND MHC I RECEPTOR. ALSO, THIS BINDING REQUIRES CO-RECEPTOR CD8 EXPRESSED BY T-CELL WHICH BINDS TO ALPHA 3 OF MHC CHAIN. CD3 THEN TRIGGERED, COMPLETING SIGNAL 1

    SIGNAL 2 INVOLVES CO-STIMULATORY MOLECULES (CD28 ON T-CELL AND CD80/86 (B7) ON APC)

    SIGNAL 1 IN ABSENCE OF SIGNAL 2 CREATES ANERGY

    ONCE ACTIVATED, T-CELLS DO NOT NEED SIGNAL 2
  43. WHAT IS A REQUIRED GROWTH FACTOR FOR T-CELLS?
    THE CYTOKINE INTERLEUKIN 2 (IL-2) IS REQUIRED FOR GROWTH AND ALSO SUSTAINED ACTIVATION

    PRODUCED BY CD4 SUBSET CELLS TH1
  44. WHAT ARE SOME ENZYMES AND LIGANDS ASSOCIATED WITH APOPTOSIS?
    CASPASE AND CASPASE-ACTIVATED DNase (CAD) CAUSE DNA FRAGMENTATION

    GRANZYMES ARE CYTOPLASMIC GRANULES WHICH MIGRATE TOWARD TARGET CELL AFTER BINDING AND ENTER THROUGH PORES CREATED BY PERFORIN AND ENTER INTO CASPASE PATHWAY

    PERFORIN INCALATES INTO THE LIPID BILAYER OF PLASMA MEMBRANE TARGET CELL CREATING LARGE PORES

    FAS LIGAND EXPRESSED ON CTLs IS RELATED TO THE CYTOKINE TUMOR NECROSIS FACTOR-ALPHA (TNF-A). AFTER DUAL RECOGNITION, FAS LIGAND ENGAGES FAS ON TARGET CELL AND INITIATES CASPASE CASCADE
  45. DESCRIBE CHARACTERISTICS OF NATURAL KILLER CELLS
    CONSIDERED PART OF THE INNATE DEFENSE SYSTEM

    CONTAIN MANY CYTOPLASMIC GRANULES AND ARE SOMETIMES REFERED TO AS LARGE GRANULAR LYMPHOCYTES (LGLs)

    DO NOT RECOGNIZE ANTIGENS AND PREFERENTIALLY ATTACK HOST CELLS THAT LACK MHC I RECEPTORS.
  46. WHAT ARE 2 REQUIREMENTS FOR ANTIBODY-MEDIATED IMMUNITY?
    1) APC TO PROCESS AND PRESENT EXTRACELLULAR ANTIGENS VIA MHC II RECEPTORS

    2) HELPER T-CELLS TO UPREGULATE B-CELLS AND THUS PLASMA CELLS
  47. 5 BASIC STEPS IN EXOGENOUS PROCESSING OF ANTIGEN
    1) PHAGO/ENDOCYTOSIS OF ANTIGEN

    2) FUSION OF VESICLE WITH LYSOSOMES

    3) FUSION OF VESICLES CONTAINING DIGESTED FRAGMENTS AND VESICLES CONTAINING MHC II RECEPTORS FROM GOLGI

    4) PARTIAL DIGESTION OF INVARIANT CHAIN PLUGGING UP MHC II LEAVING CLASS II ASSOCIATED INVARIANT CHAIN PEPTIDE (CLIP)

    5) CLASS II MOLECULE HLA-DM REMOVES CLIP AND ALLOWS BINDING OF ANTIGEN AND MHC II
  48. BASIC STRUCTURE OF MHC II RECEPTORS
    2 ALPHA AND 2 BETA SEGMENTS CREATING HETERODIMER

    ALPHA 1 AND BETA 1 PROVIDE SITE FOR ANTIGEN BINDING

    3 ISOFORMS (HLA-DP, HLA-DQ, AND HLA-DR)

    ALPHA CHAINS FOR DP, DQ, AND DR

    BETA CHAINS FOR DP, DQ, AND 2 FOR DR

    DIMER CREATED FROM 1 ALPHA AND 1 BETA CHAIN

    NO RECOMBINATION

    WITH 2 BETA DR FORMS, MHC II HAS TOTAL OF 8 DIFFERENT POTENTIAL MOLECULES COMPARED TO 6 MHC I
  49. NAME THE CYTOKINES PRODUCED FROM TH1 AND THEIR FUNCTIONS (4)
    IL-2 SUPPORTS T-CELL GROWTH AND SUSTAINED ACTIVATION

    IFN-GAMMA ENHANCES INFLAMMATION, ACTIVATES PHAGOCYTES, SUPPRESSES TH2 RESPONSES. PROMINENT PRODUCT OF NK CELLS, WHICH AMPLIFIES TH1-CELL ACTIVATION AND DAMPENS TH2-CELL ACTIVATION

    TNF-ALPHA ENHANCES INFLAMMATION, INCREASES VASCULAR PERMIABILITY

    IL-3 STIMULATES HEMATOPOIESIS
  50. NAME THE CYTOKINES PRODUCED BY TH2 AND THEIR FUNTIONS (5)
    IL-3 STIMULATES HEMATOPOIESES

    IL-4 B-CELL ACTIVATION AND GROWTH, IgE ISOTYPE SWITCH, SUPPRESSES TH1/TH17 RESPONSES

    IL-5 B-CELL DIFFERENTIATION, SUPPRESSES PRODUCTION OF TH1 CYTOKINES

    IL-10 B-CELL DIFFERENTIATION, SUPPRESSES PRODUCTION OF TH1 CYTOKINES

    TGF-BETA B-CELL DIFFERENTIATION, SUPRESSES PRODUCTION OF TH1 CYTOKINES

    *THINK EXTRACELLULAR RESPONSE
  51. NAME THE CYTOKINE PRODUCED BY TH17 AND ITS FUNCTIONS
    IL-17 INDUCES CHEMOKINES FOR NEUTROPHIL RECRUITMENT, INDUCES IL-6, INDUCES ACUTE PHASE PROTEINS, SYNERGIZES WITH IFN-GAMMA AND TNF-ALPHA
  52. IL-1 ORIGIN AND EFFECT
    MACROPHAGES

    INITIAL STAGES OF T-CELL GROWTH, FEVER
  53. IL-6 ORIGIN AND EFFECT
    MACROPHAGES & T CELLS

    GROWTH AND DIFFERENTION OF NUMEROUS LEUKOCYTES, PROMINENT IN INDUCTION OF ACUTE PHASE PROTEINS
  54. IL-12 ORIGIN AND EFFECTS
    DENDRITIC CELLS AND MACROPHAGES

    STIMULATES NK CELLS TO PRODUCE IFN-GAMMA

    INHIBITS TH17 DIFFERENTIATION

    IL-23 PROMOTES TH17 DIFFERENTIATION
  55. IL-23 ORIGIN AND EFFECTS
    DENDRITIC CELLS

    STIMULATES TH17 CELLS TO PRODUCE IL-17
  56. TNF-ALPHA ORIGINS AND EFFECTS (TNF-a)
    TUMOR NECROSIS FACTOR

    MACROPHAGES, NK CELLS, TH1 CELLS

    ENHANCES INFLAMMATION, INCREASES VASCULAR PERMEABILITY, CYTOTOXIC FACTOR
  57. GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR (GM-CSF) ORIGINS AND FUNCTIONS
    MACROPHAGES, T-CELLS

    STIMULATES GROWTH AND DIFFERENTIATION OF MYELOID LINEAGE
  58. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
    ASSOCIATED WITH VARIETY OF CAUSES INCLUDING INFECTION

    SEPSIS SYNDROME IS EXCESSIVE RELEASE OF INFLAMMATORY MEDIATORS DUE TO INFECTION REULTING IN ENDOTHELIAL DAMAGE, HYPOTENSION, POORLY REGULATED COAGULATION THAT CAN LEAD TO IRREGULAR HEARTBEAT (TACHYCARDIA), AND EVENTUAL MULTI-ORGAN FAILURE

    ASSOCIATED WITH DISSEMINATED INTRAVASCULAR COAGULATION RELATED TO BACTERIA

    SEPTIC SHOCK
  59. SUPERANTIGENS
    PRODUCED BY MICROBIAL PATHOGENS THAT ACTIVATE LARGE NUMBERS OF T CELLS WITH PRO-INFLAMMATORY CAPABILITIES (ex TH1/TH17 CHARACTERISTICS)

    RESPONSIBLE FOR A VARIETY OF CLINICAL CONDITIONS ASSOCIATED WITH SHOCK, INCLUDING TOXIC SHOCK SYNDROME AND FOOD POISONING

    ACTIVATE T CELLS INDEPENDENT OF THEIR ANTIGEN SPECIFICITY DUE TO BINDING OUTSIDE OF POLYMORPHIC ANTIGEN BINDING REGIONS
  60. GRANULOMA FORMATION
    CLUSTER OF INFECTED MACROPHAGES WHICH ARE WALLED OFF BY T CELLS (ex MYCOBACTERIUM TUBERCULOSIS)

    MIROORGANISMS WHICH ARE ABLE TO SURVIVE INGESTION INTO PHAGOCYTES LEAD TO CONTINUOUS EXOGENOUS PROCESSING AND MHC II PRESENTATION

    THIS CAUSES RELEASE OF IFN-GAMMA AND TNF-ALPHA WHICH FURTHER ACTIVATES INFECTED MICROPHAGES, RESULTING IN TH1 --> MACROPHAGE --> TH1 LOOP.
  61. T-REGS
    REGULATORY T CELL CAPABLE OF MODULATING CYTOKINE LEVELS AND PREVENTING EXCESSIVE INFLAMMATION

    IDENTIFIED BY HIGH EXPRESSION OF IL-2 RECEPTOR CD25 AND TRANSCRIPTIONAL ACTIVATOR foxP3 WHICH HELPS PRODUCE INFLAMMATION-SUPPRESSIVE CYTOKINES
  62. LINKED RECOGNITION
    HOW B CELLS COMMUNICATE WITH T CELLS

    B CELLS BIND EXOGENOUS ANTIGEN TO SURFACE RECEPTOR, WHICH IS THEN INTERNALIZED

    ANTIGEN IS PROCESSED VIA ACIDIFIED ENDOSOES AND FRAGMENTS CHANNELED INTO EXOGENOUS PROCESSING PATHWAY (MHC II PRESENTATION)

    TH2 CELLS ARE ACTIVATED, GIVING CO-STIMULATORY SIGNALS BACK TO B CELLS (CD40/CD40L)
  63. THP OR TH0 CELLS
    PROGENITORS OF THE OTHER EFFECTOR CD4+ T CELLS. CAN PRODUCE IL-2 THAT HELPS DRIVE THEIR OWN EXPANSION VIA AN AUTOCRINE STIMULATION

    APPEAR TO BE REGULATED BY CELLS OF THE INNATE IMMUNE SYSTEM (APCs DETERMINE WHICH CYTOKINES ULTIMATELY PRODUCED)

    COMPOSITE CYTOKINE ENVIRONMENT WILL DETERMINE WHICH T CELL SUBSET WINS, THOUGH OFTEN IT'S A COMBINATION
  64. THP --> TH1
    IFN-GAMMA WHICH COMES FROM NK CELLS ACTIVATED BY IL-2 PRODUCED BY DENDRITIC CELLS AND MACROPHAGES.

    NEW TH1 CELLS ALSO PRODUCE IFN-GAMMA WHICH HELPS INHIBIT TH2 CELLS
  65. THP --> TH2 CELLS
    IL-4 IN ENVIRONMENT OF LOW IFN-GAMMA STARTS INITIAL CONVERSION TO TH2 CELLS

    NEW TH2 CELLS PRODUCE MORE IL-4 THUS MAKING MORE TH2 CELLS

    TGF-BETA AND IL-10 MADE BY TH2 CELLS INHIBIT PROLIFERATION OF TH1 CELLS
  66. THP --> TH17
    IL-6 PLUS TGF-BETA IN LOW ENVIRONMENTAL IFN-GAMMA AND IL-4

    DENDRITIC-CELL-DERIVED IL-23 EXPANDS TH17 DIFFERENTIATION BUT CAN ALSO RELEASE IL-12 THAT INHIBIT

    DENDRITIC CELLS DETERMINE IF TH1 OR TH17 CELLS ARE MADE
  67. GAMMA-DELTA T-CELLS
    EXPRESS GAMMA-DELTA CHAINS ON RECEPTORS INSTEAD OF ALPHA-BETA

    LOCATED PRIMARILY IN SKIN AND MUCOSAL LAYERS

    PROVIDE EARLY ADAPTIVE IMMUNITY, PARTICULARLY BY PRODUCING IMPORTANT CYTOKINES

    RECOGNIZES SPECIALIZED NON-POLYMORPHIC SURFACE MOLECULE CD1 INSTEAD OF MHC I OR II

    CD1 RESEMBLES MHC I ALTHOUGH IR PRESENTS LIKE MHC II VIA THE EXOGENOUS PATHWAY

    CD1 SPECIALIZES IN PRESENTING GLYCOLIPIDS AND PHOSPHOLIPIDS COMMON TO THE MEMBRANES OF MANY BACTERIAL PATHOGENS

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