y1 lecture 1717 julai 2007

Upload: cikgubaru

Post on 10-Apr-2018

241 views

Category:

Documents


0 download

TRANSCRIPT

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    1/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    2/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    3/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    4/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    5/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    6/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    7/35

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    8/35

    Account for 0.5% of WB Cs an d: Have U- or S-sha ped nuclei with tw o or three

    cons picuous c onstricti ons Are f uncti onally si milar t o mast cells Have large, pur plish-black (bas ophilic)

    granules that c ontain hista mineHistamine in f lamm atory che mical that acts as avas odilator an d attracts other WB Cs (antihista minescounter this e ff ect)

    Bas ophils

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    9/35

    Agranulocytes ly mphocytes an d monocytes: L ack visible cyt op lasmic granules Are si milar structurally, but are f uncti onally

    distinct an d unrelate d cell ty pes

    Have s pherical (ly mp hocytes) or kidney-sha ped (mo nocytes) nuclei

    Agranul ocytes

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    10/35

    Account for 25% or mo re of WB Cs an d: Have large, dark- pur ple, circular nuclei with a

    thin ri m of blue cyt op lasm Are found mo stly en meshe d in ly mphoid tissue

    (some circulate in the bl ood )There are tw o ty pes of lymphocytes: T cellsand B cells T cells f uncti on in the i mm une res ponse B cells give rise t o plasma cells, which pr oduce

    antib od ies

    L ymphocytes

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    11/35

    Monocytes acc ount for 48% of leuk ocytes They are the largest leuk ocytes They have abun dant pale-blue cyt op lasms They have pur ple-staining, U- or kidney-sha ped

    nuclei

    They leave the circulati on, enter tissue, an d diff erentiate int o macr ophages

    Monocytes

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    12/35

    Macr ophages: Are highly mo bile an d actively phag ocytic Activate ly mp hocytes t o mo unt an i mm une

    res ponse

    Monocytes

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    13/35

    Summ ary of For med Ele ments

    Table 17.2

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    14/35

    Summ ary of For med Ele ments

    Table 17.2

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    15/35

    L euk opo iesis is h or monally sti mulate d bytwo f amilies of cytokines (he matopo ieticf actors) interleukins an d colony-stimulating f actors ( CSFs) Interleukins are nu m bere d (e.g., I L -1, I L -2),

    whereas CSFs are na med for the WB Cs theystimulate (e.g., granul ocyte- CSF sti mulatesgranul ocytes)

    Macr ophages an d T cells are the mostimpo rtant s ources of cytokinesMan hemato oietic h or mones are use d

    Pr oducti on of L euk ocytes

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    16/35

    For mation of L

    euk ocytes

    Figure 17.11

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    17/35

    The Immune SystemDefends body against pathogens

    Can distinguish between self and non-self

    General Defence System (innate)Non-specific = acts against all pathogensRapid

    1. First line of general defenceSkin = barrier. Sweat (acidic pH)Clotting = also helps protect skinLysozyme = enzyme in saliva, sweat, tears. Attacks bacterial cell walls

    Mucous (respiratory, digestive, urinary & reproductive tracts) = traps pathogensCilia= little hairs that help clear mucous (and pathogens) from respiratory tractAlimentary canal = lysozyme in saliva, stomach HCl kills many pathogens, specialisedimmune areas in the GI tract, very high turnover of epithelial cells, antibodies

    Specific Defence System (adaptive)

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    18/35

    2 . Second line of general defencePhagocytic white blood cells (leukocytes) = destroy pathogens that enterComplementInflammation

    Phagocytes ( Phago= eat; cyte=cell)attracted to a site of infection ( chemotaxis ) by chemicals released by injured cellsThree types neutrophils (short lived),

    monocytes (short-lived..in blood) and macrophages (long-lived..in tissue)

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    19/35

    Macrophages very large white cells that can move

    around body, or remain in certain tissues. Long lived,act as scavengers

    Immune organs

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    20/35

    Complementset of 30 proteins found in plasma that are activated by

    infectioncomplicated chain reaction that leads to the bursting ofviruses and bacteria

    made in the liver

    Interferonsset of proteins produced by virally infected cells cells to limit the spread of viral

    infections, by inducing a state of resistance in healthy cells.induced by viruses, bacteria and other signals from the immune system

    Inflammationinfected cells ( mast cells ) release histamine , which is a vasodilator . This causeslocalised swelling, redness, heat, pain. Can also cause high temperature.

    brings white cells to the area of infectionAnti-histamines

    2 . Second line of general defence cont.

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    21/35

    Comp lement Pathways

    Figure 21.5

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    22/35

    Inter f er on (IFN)

    Figure 21.4

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    23/35

    N eutrophilsenter blood

    from bonemarrow

    1

    2

    3

    4

    Margination

    Diapedesis

    Positive

    chemotaxis

    Capillary wallEndotheliumBasal lamina

    Inflammatorychemicalsdiffusing fromthe inflamedsite act aschemotacticagents

    n amm a ory es ponse: ag ocy cMo bilizati on

    Figure 21.3

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    24/35

    Red bone marrow

    1

    2

    3

    Immunocompetent,but still naive,lymphocytemigrates via blood

    Mature (antigen-activated)immunocompetent lymphocytescirculate continuously in thebloodstream and lymph andthroughout the lymphoid organs of the body.

    Key: = Site of lymphocyte origin

    = Site of development of immunocompetence

    as B or T cells; primary lymphoid organs= Site of antigen challenge and final

    differentiation to activated B and T cellsImmaturelymphocytesCirculation in

    blood 11 Lymphocytes destined to become T

    cells migrate to the thymus and developimmunocompetence there. B cellsdevelop immunocompetence in redbone marrow.

    ThymusBone

    marrow

    Lymph nodes,spleen, and other lymphoid tissues

    2 2 After leaving the thymus or bonemarrow as naive immunocompetentcells, lymphocytes seed the lymphnodes, spleen, and other lymphoidtissues where the antigen challengeoccurs.

    3 3

    ActivatedimmunocompetentB and T cellsrecirculate in bloodand lymph

    Imm unocomp etent B or T cells

    Figure 21.8

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    25/35

    Major r olls in i mmunity are: To engul f foreign particles

    To present f rag ments of antigens on their ownsur f aces, t o be rec ognize d by T cells

    Major AP Cs are dendritic cells (D Cs),macr ophages, an d activate d B cellsThe major initiat ors of ada ptive i mm unityare D Cs, which actively migrate t o thelymph nodes an d secondary ly mphoid

    organs an d present antigens t o T an d B cells

    Antigen-Presenting Cells (AP Cs)

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    26/35

    Secrete soluble pr oteins that activate T cellsActivated T cells in turn release che micalsthat: Rev u p the maturati on an d mo bilizati on of DCs Pr od macr ophages t o bec om e activate d

    macr ophages, which are insatiable phag ocytesthat secrete bacterici dal che micals

    Macr ophages an d Den dritic Cells

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    27/35

    Specific Defence System (Adaptive Immune System)

    Antigens foreign molecules thatgenerate anti body production

    Antibodies (immunoglogulins) proteinsproduced by lymphocytes in responseto antigens

    Monocytes develop into macrophages which phagocytose foreign particles ( antigens )Lymphocytes -

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    28/35

    IgD mo nomer attache d to the sur f ace of B cells,impo rtant in B cell activati onIgM penta mer release d by plasma cells duringthe primary i mm une res ponse

    IgG

    mo nomer that is the mo st abun dant an d diverse antib ody in primary an d sec ondaryres ponse; cr osses the placenta an d conf ers passiveimm unityIgA dimer that hel ps prevent attach ment of

    pathogens t o e pithelial cell sur f acesIgE monom er that bin ds to mast cells an d

    bas ophils, causing hista mine release whenactivate d

    Classes of Antib od ies

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    29/35

    Mechanis ms of Antib ody Acti on

    Figure 21.13

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    30/35

    Maj or Ty pes of T Cells

    Figure 21.14

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    31/35

    T-lymphocytes

    Helper T-CellsRecognise antigens on

    surface of leukocytes,especially macrophages

    Enlagre and form aclone of T-helper cells

    Secrete interferon andcytokines whichstimulate B-cells andstimulate killer -cells

    Can be infected by HIV

    Killer T-CellsAlso called cytotoxic

    Destroy abnormal bodycells, e.g. virus infectedor cancer cells

    Stimulated by cytokines(THcells)

    Release perforin , whichforms pores in targetcells. This allows waterand ions in = lysis

    Suppressor T-CellsControl the

    immune systemwhen the antigen/pathogen hasbeen destroyed

    Only recentlydiscovered solittle is knownabout them

    Memory T-CellsCan survive a long tim

    and give lifelongimmunity frominfection

    Can stimulate memoryB-cells to produceantibodies

    Can trigger productionof killer T cells

    Mature in Thymus, which is most active just before and after birth.The thymus starts to shrink during puberty.

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    32/35

    Abnormal cell e.gcancer cell, infected cell

    Normal cell

    Antigen

    Killer T-cellrecognises antigen

    Clones of killer T-cellattach to antigen

    Helper T-cell stimulatescorrect killer T-cell to

    multiply

    Killer T-cells releaseperforin pores

    Abnormal cell gainswater, swells andbursts

    Helper T-cell alsostimulates B-cellsto make antibodies

    Memory T-cells stay incirculationSuppressor T-cellsturn off immune

    response

    X X

    X

    How T-cells work

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    33/35

    Duration of immunityMemory B-cells circulate for a long time. If the same pathogen infects thebody again, these B-cells can produce large amounts of specific antibodyvery quickly. This is why you usually dont suffer from the same infectiontwice.Memory T-cells survive a long time and trigger an immune response

    Tumours in most cases the body recognises tumours as being bad, because theyexpress abnormal molecules on the cell surface. However sometimes the body doesntnotice and cancers can develop

    Immune disordersSometimes the body produces antibodies against its own tissues e.g. autoimmunediseases e.g. rhumatoid arthritis, Crohns disease, SCID (bubble boy disease),

    asthma

    Allergies occur when the body reacts to materials which should notbe antigenic e.g. peanuts

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    34/35

    Induced Immunity

    Active immunityProduction of a persons ownantibodies. Long lasting

    Passive immunityAn individual is given antibodies by anotherShort-term resistance (weeks- 6months)

    Natural ActiveWhen pathogen

    enters body in the

    normal way, wemake antibodies

    Natural PassiveBaby in utero

    (placenta)

    Breast-fed babies

    Artificial PassiveGamma globulin

    injection

    Extremely fast, butshort lived (e.g. snakevenom)

    Edward Jenner

    Artificial ActiveVaccination usually

    contains a safe antigen

    from the pathogen.Person makesantibodies without

    becoming ill

    yumm y

  • 8/8/2019 y1 Lecture 1717 Julai 2007

    35/35

    Overview of the Immune Response