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Chapter 11. Immune response (1)

Chapter 11. Immune response (1). I. Introduction II. Antibody-mediated Humoral Immunity. I. Introduction. 1. Concept of Immune Response 2. Types of Immune Response 3. Process of Immune Response. 1. Immune response.

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Chapter 11. Immune response (1)

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  1. Chapter 11. Immune response (1) I. Introduction II. Antibody-mediated Humoral Immunity

  2. I. Introduction 1. Concept of Immune Response 2. Types of Immune Response 3. Process of Immune Response

  3. 1. Immune response The immune system of body is able to recognize subtle chemical differences that distinguish one foreign pathogen from another. At the same time, the system is able to discriminate between foreign molecules and the body’s own cells and proteins. Once a foreign organism is recognized, the immune system eliminate or neutralize the organism, finally.

  4. 2. Types of Immune ResponseAutoimmunity selection Immune “Self”Ag Autoimmune ToleranceAg system: activation “non-self”Ag HI / CMI Immune Tolerance Hypersensitivity Reaction

  5. II. Antibody-mediated Humoral Immunity concept of HI ，simple process of HI 1. Common rule of Ab production 2. Interaction between immune cells in process of producing Ab 3. Immune Memory 4. Effect of Humoral Immunity

  6. Humoral Immunity，HI Humoral immunity is mediated by antibodies of various different classes; which Ab are produced by cells of the B cell lineage in response to stimulation by Ag.

  7. Simple process of HI: 1、TD—Ag APC TH BL2 THmBLm 2、TI—Ag BL1 Mature B cell Plasma cells Ab HI

  8. 1.Common rule of Ab production a. The regularity of Ig production in phylogenic evolution and development,and ontogenesis. b. The regularity of Ab production in the primary and secondary response。

  9. Secondary Immune Response When the immunized individual after a primary contact with antigen is injected by a second injectionof the same antigen, production of antibody becomes apparent, this response is called the secondary response.

  10. Primary IR Secondary IR Antigen The first contact of an A second injection of the individual with an Ag same Ag latent period long (1W，2-3W) short (1-3day) slow of Ab production Ab Conc. low in serum high in serum Maintain Time short,decrease quickly longer type of Ig IgM IgG Affinity lower higher present of Ag M, DC B cell

  11. Ig IgM IgG Concentration of Ig Latent period Secondary stimulation of Ag 10day 3day Primary stimulation of Ag

  12. 2. Interaction between immune cells in the process of producing Ab TD—Ag response a. Interaction between M and Th cells * M presented Ag *Interaction between cells b. Interaction between Th cell and B cells * B cell presented Ag * Interaction betweencells c. Interaction between M and B cells TI—Ag response B cell : response of TI—Ag

  13. Ags are ingested, processed, presented by M (primary response) • Ingestion：endocytosis, passive adhesion。 • Processing：lysosomal enzymes condense and degrade Ag,and combine to self-MHCII molecules. • Presentation：These complexes of peptide and MHC molecules are transported to the surface of the cell where they are recognized by the T-cell receptor.

  14. Exogenous Ag endocytosis degradation endosome TCR expression CD4 MHCII combination Transportation APC

  15. Virus（endogenous Ag） DNA transcription mRNA translation Pr degradation CD8 CTL TCR MHCI Target cell

  16. Interaction between M and Th cells （primary response） Double signal hypothesis of Th cell activation ： The first signal ： Th: TCR/CD3——APC: Ag-MHCII complexes at the same time, TH: CD4——APC: The 2,2 domain of MHCII The second signal ： APC: B7/BB1（CM）——TH: CD28（CMR） TH secreted IL-2 and expressed IL-2R Finally cells divide, clones proliferation, and produce a kind of CK.

  17. TH (CMRs) CD28 CTLA4 APC (CMs) CD2 CD58 B7/BB1 CD3 Ag MHC-II TCR ICAM-1 LFA-1 IL-2 CD4 VCAM-1 VLA-4 IL-2R Signal 1 Cell activation,（CK） cell differentiation and clone proliferation Signal 2 Interaction between APC and Th cell

  18. APC APC B7/BB1 • MHC-Ag TCR/CD3 CD28 Signal 1 Signal 2 Signal 2 Signal 1 TH TH IL-2 production clone proliferation notIL-2 production clone anergy

  19. Suppressive immune response ： Hypersensitivity Disease Autoimmunity Disease Graft rejection responses Ag APC TH MHC TCR inactivation B7 CD28 Anti-B7Ab CTLA4 Ig Anti-CD28 • Interdiction of co-stimulatory signals

  20. Enhancing immune response： Tumor immunity treatment Ag MHC TCR CTL Tumor cell signal1 CTL activated Killer tumor cell signal2 CD28 B7 Ag MHC CTL TCR Tumor cell signal1 CTL activated Killer tumor cell signal2 CD28 Transfection B7gene

  21. Interaction between Th and B cells（secondary response） Th cell activation： Double signal hypothesis Signal 1：Th: TCR/CD3——B cell: Ag-MHCII complexes Th: CD4——B cell: The 2,2 domain of MHCII Signal 2：Th: CD28 molecule ——B cell: B7 molecule. B cell activation： Double signal hypothesis Signal 1：B cell: BCR--Ag，Ig,Ig transfer activation signal 1 Signal 2：B cell: CD40——Th: CD40L Th and B cell inducing signal of activation each other，Th produced IL-4,5,6. B cell is helped at Th cell, finally B cell proliferated and differentiated turn into the plasma cells of producing a kink of Igs.

  22. B cell T cell ICAM-1 LFA-1 Ag CD3 B7 Signal 2 CD28 SIg CD3 Ag process MHC-II Signal 1 TCR present 1 CD4 2 CD40 CD40L singal LFA-1 ICAM-1 CKR B cell activation CK Th activation Interaction between B cell and T cell

  23. M M process present MHC-II TCR ingestion Ag IL-2，4，5，6 IL-1 PC Activate Th ingestion TCR IgM IgG MHC-II IgA IgE B B process differentiation Bm present B B proliferation Activate B Bm Bm Bm Bm c. Interaction between M and B cells

  24. signal signal B cell B cell I type: TI—Ag is polyclonal stimulator II type: multiple repeat-lined antigenic determinant makes receptor linkage TI-Ag response

  25. 3. Immune Memory-Secondary response Characteristic : a. Immune memory cells b. Class switching of Ig c. Affinity Maturation of Ab

  26. Characteristic： *Immune memory cells: THm Bm * Involved in Humoral immunity and cell-mediated immunty. * Ab conc. increases，class switching of Ab， and affinity maturation of Ab

  27. 4. Effect of Humoral Immunity • Neutralization of Ab • Opsonization of Ab • Complement dependent cell-mediated cytotoxicity,CDC • Antibody dependent cell-mediated cytotoxicity,ADCC • Immune regulation of Ab

  28. FcrR Anti-bacteria Ab Bacteria M Boost up lick up action Opsonization of Ab

  29. Surface Ag FcrR IgG Target cell M , NK Dissolution of target cell Antibody-dependent cell-mediated cytotoxicity, ADCC

  30. Chapter12. Immune response (2) I. Introduction II. CD4 T-mediated immunity III.CD8 T-mediated immunity

  31. I. Introduction 1. Concept, Simple process 2. Major functions of CMI

  32. Simple process: secondary TDTH CK TD-Ag Immune system Tc Cytotocixity

  33. 2. Major Functions of CMI • Delayed Type Hypersensitivity, DTH • Intracellular Anti-infection • Anti-tumor • Transplantation rejection reaction • Graft Versus Host Reaction, GVHR • Autoimmunity diseases

  34. II. CD4 T-mediated immunity 1. Activation of CD4 T cells 2. Formation of DTH inflammation * CK production * Function of M

  35. Activation of CD4 T cells Double signal hypothesis of CD4 T cell activation ： The first signal ： Th: TCR/CD3——APC: Ag-MHCII complexes at the same time, TH: CD4——APC: The 2,2 domain of MHCII The second signal ： APC: B7/BB1（CM）——TH: CD28（CMR） TH secreted IL-2 and expressed IL-2R Finally cells divide, clones proliferation, and produce a kind of CK.

  36. IL-2R IL-2R APC (CMs) TH (CMRs) CD2 CD58 CD28 CTLA4 B7/BB1 CD3 MHC-II Ag TCR Signal1 CD4 Signal 2 ICAM-1 LFA-1 VLA-4 VCAM-1 IL-2 IL-2R Cell activation,（CK） cell differentiation and clone proliferation

  37. IL-2 TNF APC APC APC T T T T T T T T IFNr rest activation CK of DTH reaction M M

  38. III.CD8 T-mediated immunity 1. Activation ofCD8 T cells 2. Mechanisms of Tc killing target cells a. Perforin b. Granzymes c. TNF associated proteins

  39. Activation of CD8 T cells Double signal hypothesis of CD8 T cell activation ： The first signal ： Tc: TCR/CD3——Target cell: Ag-MHC-I complexes at the same time, Tc: CD4——Target cell: The 3 domain of MHC-I The second signal ： Target cell: B7/BB1（CM）——Tc: CD28（CMR） Tc secreted IL-2 and expressed IL-2R Finally cells divide, clones proliferation, and secrete effect molecules.

  40. CTLA4 Tc (CMRs) CD2 CD58 B7/BB1 Target cell (CMs) CD3 Ag MHC-I TCR ICAM-1 LFA-1 IL-2 IL-2R Cell activation, differentiation , clone proliferation and secreted effect molecules. Signal 1 CD8 Signal 2 Interaction between target cell and Tc

  41. Ag recognition Tc activation Tc killed target cell Target cell died Tc unbind

  42. TCR Rest Tc Target cell MHCI IL-2，IL-6，IFN APC TH1 MHCII death Effector Tc Target cell

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