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MindMap Gallery Medical Immunology Chapter 16 Immune Tolerance

Medical Immunology Chapter 16 Immune Tolerance

Medical Immunology Chapter 16 Immune Tolerance Mind Map, including the formation of immune tolerance, immune tolerance mechanism, immune tolerance and clinical medicine, etc.

Edited at 2023-12-13 16:11:44

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Medical Immunology Chapter 16 Immune Tolerance

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Outline

Chapter 16 immune tolerance (IT)

Overview

T/B cells cannot produce specific immune effector cells and/or antibodies when exposed to a specific antigen. The phenomenon of normal response to stimulation of other tolerogens is also called "negative immune response"

and immune response complement each other, and the balance between the two is crucial to maintaining immune homeostasis

Section 1 The development of immune tolerance

1. Natural immune tolerance (congenital IT) Embryonic development, immature lymphocytes → exposure to antigen → loss of response to antigen after birth

2. Immune tolerance caused by acquired exposure to antigens (acquired, acquired IT) Mature lymphocytes → activation disorder, regulatory T cells, etc. → lose response to antigens

Antigenic factors

1. Antigen dose

Low-band tolerance: The antigen dose is too low to activate T and B cells and cannot induce immune response.

High-band tolerance: The antigen dose is too high, which may induce cell apoptosis or inhibit immune response toward regulatory T differentiation.

B cell, T cell tolerance

High-dose TI antigen - induces B cell tolerance (high-band tolerance)

High-dose TD antigen - induces B cell tolerance (high-band tolerance)

High/low dose TD antigen - T cell tolerance (low band tolerance/high band tolerance)

Compared

T cells: easier to form The amount of antigen required is smaller than that of B cells It happens quickly (peak within 241 days) Lasts long (months to years)

B cells: more difficult to form A large amount of antigen is required Occurs slowly (1 to 2 weeks) Lasts short (several weeks)

2. Antigen type and dosage form

Protein monomers are not easily taken up by APC and presented to T cells → T cells cannot assist B cells to produce corresponding antibodies.

Protein monomer adjuvant → easily absorbed by APC to induce normal immune response

3. Antigen immunity pathway

Tolerance level: oral > intravenous injection > intraperitoneal injection > intramuscular injection > subcutaneous and intradermal injection

Oral—separation tolerated Intestinal CD4 T cells stimulate TGE-β and IL-4 → induce B cells to produce IgA to exert local immune effects on the mucosa, Induction of regulatory T cells leads to systemic immune tolerance

4. Antigen persists Lack of APC to provide the second signal, repeated stimulation by antigens can easily lead to T cell apoptosis after activation (meaning: interval immunity)

5. Antigenic epitope characteristics (chicken egg lysozyme HEL)

The N-terminal epitope of HEL (tolerogenic epitope) → induces Treg cell activation (immune tolerance)

The C-terminal epitope of HEL → induces Th activation (immune response)

body factors

Age and developmental stage: embryonic stage>neonatal stage>adult animal

Physiological state: antigen induction immunosuppressant

genetic background

Section 2 immune tolerance mechanism

Central tolerance (negative selection) (Tolerance formed by encountering self-antigens during the development of T and B cells in central immune organs (thymus, bone marrow) during the embryonic period and after birth)

(1) T cell central tolerance Location: Thymus Stage: Immature single-positive T cells

mechanism Negative selection: Immature single-positive T cell TCR binds to self-PMHC

Gaoxinheli→→Apoptosis (clone removal)

Medium affinity →→ Naturally occurring T cells (nTreg) generation

(2) B cell central tolerance Location: bone marrow Stage: Immature B cells

mechanism Negative selection: In the bone marrow, immature B cells BCR binds with their own Ag with high affinity and then undergoes apoptosis (clonal clearance) or receptor editing, incompetence, etc.

peripheral tolerance (Mature T and B cell clones do not produce a positive immune response when encountering endogenous (self) or exogenous (non-self) antigens and show tolerance)

(1) Clone removal Meaning: The process in which T/B cells bind to high-affinity Ag at high concentrations and are induced to undergo apoptosis. mechanism: T cells: Fas/FasL-mediated activation-induced apoptosis (AICD) B cells: Th cells do not provide the second signal for B cell activation

(2) Immune neglect

Meaning: The immune system does not respond to low-level or low-affinity antigens

Mechanism: Lack of the first signal of T/B cell activation

(3) Cloning incapacity

Meaning: T and B cells show inactivation when stimulated by Ag.

mechanism

T cell anergy: Immature DCs express low costimulatory molecules and cannot produce IL-12, and cannot provide a second signal for T cell activation. T cells cannot be fully activated, but are induced into a state of clonal anergy, and then become unresponsive to antigen stimulation in the presence of a second signal.

B cell incompetence: Th (T helper cell, second signal) is incapacitated, and B cells cannot be effectively activated; Monomeric soluble Ag has no cross-linking effect (cross-links BCR, first signal)

(4) The role of immune regulatory cells

Naturally occurring nTregs in developing thymic C: direct contact with target cells

Peripherally induced iTreg: secrete IL-10, TGF-β and other cytokines to exert immunosuppressive functions

(5) Antigens at immune privileged sites

Immunoprivileged sites: Anatomically isolated from immune cells or mechanisms that suppress immune responses exist in the local microenvironment Brain, spinal cord, eye lens, placenta/uterus, testicles

①Physiological barrier ② Locally induce immune deviation and inhibit Th1 type response ③Express FasL and induce apoptosis of Fas lymphocytes ④Production of TGF-β inhibitory cytokines

Section 3 Immune tolerance and clinical medicine

Establish immune tolerance (Hypersensitivity, autoimmune disease, transplant rejection)

1. Oral or intravenous injection of antigen

Oral Ag: "Tolerance to Dissociation"

Intravenous donor allotype Ag

2. Soluble Ag or antagonist peptide (allosteric peptide)

Soluble Ag: difficult to present and induce cross-linking

Self-Ag allosteric peptide: simulates self-peptide to compete with TCR and prevent activation of T cells

3. Block costimulation signals (second signal)

Suppressive T cells: CTLA-4/Ig; anti-LFA-1 Inhibit B cells: anti-CD40L

4. Inducing immune deviation

Using cytokines to induce the deviation of lTh1/Th17 towards Th2 and inhibit the differentiation and function of Th1 and Th17 cells

5. Bone marrow and thymus transplantation

6. Adoptive infusion of suppressive immune cells

Break immune tolerance (Intrafetal infection, tumor)

1. Block immunosuppressive molecules: anti-CTLA-1, anti-PD-1 for tumor treatment

2. Activation of the second signal: activation of T cells by costimulatory molecules such as CD40

3. Inhibit Treg quantity function

4. Promote iDC maturation (immune adjuvants, stimulate TLR molecules, etc.)

5`, CK and its antibody applications

IFN-γ: Upregulates MHC class II molecules and promotes IL-12 production

GM-CSF: induces granulocyte/monocyte production and promotes DC functional maturation

TGF-β antibody: antagonizes the effect of TGF-β

autoimmune regulatory factor (AIRE) Drives many self-antigens (tissue-specific antigens) that are originally expressed only in the periphery to be ectopically expressed in epithelial cells in the thymic medullary area. AIRE deficiency→autoimmune polyendocrinopathy-candidiasis albicans-ectodermal dystrophy (autoimmune polyglandular syndrome I, APS-1)

Tolerogen - an antigen that causes immune tolerance