adaptive immunity Flashcards
(18 cards)
name the antigen-presenting cells.
- dendritic cells
- macrophages
- B-cells
describe the process whereby T-cells mature and develop from bone marrow to thymus.
- in the bone marrow the haemotatotic stem cell matures into the common lymphoid progenitor
- these then develop into thymocytes which they are now in the thymus
- in the thymus, these thymocytes undergo TCR development, positive and negative selection and then differentiate into the helper T (CD4) cells or cytotoxic T-cells (CD8), due to which MHC (I or II) its TCR recognises
- these now enter the blood and travel to secondary lymph organs
- once in the secondary lymph organs , they encounter antigen-presenting cells of which the T-cell will bind to the foreign antigen and MHC-II causing for a primary, secondary and tertiary signal - leading to the release of IL-2, IL-4, IL-5 - turning T-helper cells into Th2 (IL-4) if Th1 wanted to be made IL-12 needs to be released
describe in detail, the process of the maturation of thymocytes to T-helper and cytotoxic-T cells.
- in the thymus
- TCR development and expression
- positive selection - ensures their TCR recognises the MHC molecules, if they do, they recieve signals to continue, if they they apoptose
- negative selection - eliminates those who bind to the self - antigens on the MHC-II as they do not want autoimmune diseases
- these then differenciate into T-helper or cytotoxic-T
- if their TCR recognises MHC-II its a CD4 (T helper) if it recognises MHC-I its CD8 (cytotoxic C)
what are MHC-II and MHC-I receptors and where are they found?
- MHC-I - any nucleated cell
- MHC-II - antigen-presenting cells
outline the entire process of humeral immunity, including the names of receptors, and where in the body this occurs.
- (essentially, the macrophage activates the Th2 cells, which then in turn activates the B-cell to become activated into creating antibodies)
- macrophage enters the lymph nodes and activates the T-cells
how its activated: - macrophage B7 binds to T-cell CD28
- macrophage MHC-II binds to T-cell CD4 and foreign antigen on macrophage binds to TCR on T-cell - this whole complex activates the CD3 protein in the T-cell
- the macrophage also releases IL-1 which activates it
- the T-cell releases IL-2 - which acts autocrinely, activating itself further
- it also releases T-4 and T-5 which activates the proliferation of the T-cell into mature Th2 cells which also release IL-4 and IL-5
- B-cells take up free antigens, engulf them, and present them onto its MHC-II
- now that IL-4 has been made, it causes the B-cell to proliferate into activated B-cells which express the specific BCR for the foreign antigen (so next time antigen is detected it can bind quicker, meaning quicker proliferation into plasma cells for antibody production)
- IL-5 causes this to proliferate further into plasma or memory cells
- also some other IL but thats lowkey irrelevant
what cytokines are responsible for the activation of B-cells into plasma and memory cells?
- IL-4
- IL-5
- IL-6
- IL-10
- IL-21
explain the process of cell-mediated immunity.
- if there’s a cancerous or infected cell, it will have a self-antigen on its MHC-I and sometimes this can be displayed with a viral peptide
- the T-cell TCR will bind to the MHC-I and the T-cells CD28 will bind to the infected cells B7
- this causes the cytotoxic T-cell to release perferins and granulosomes
- perferins make holes in the infected cells membrane
- granulosomes enter these holes and activate the pro-aptotic genes
- the genes release BAX
- BAX binds to BCl2 which is a protein in the mitochondria
- once it binds, it pulls the protein out, lleaving a hole
- this causes the release of caspases which breaks down the cell
explain the T-cell antigen recognition/activation of CD8.
Steps:
Antigen Presentation:
Infected or abnormal cells present endogenous antigens (from intracellular pathogens or mutations) on MHC-I molecules.
The TCR on a naïve CD8+ T cell binds to the antigen-MHC I complex.
The CD8 co-receptor strengthens this interaction.
Co-Stimulation:
CD28 on the T cell binds to B7 (CD80/86) on the APC, providing the second activation signal.
Alternatively, cross-presentation by professional APCs can also stimulate CD8+ T cells.
Cytokine Signaling:
Cytokines like IL-2 (produced by activated T cells or nearby CD4+ helper T cells) promote the proliferation and differentiation of CD8+ T cells.
Effector Functions:
Activated CD8+ T cells differentiate into cytotoxic T lymphocytes (CTLs).
CTLs kill infected or abnormal cells by releasing:
Perforin (pore-forming protein).
Granzymes (induce apoptosis).
explain the T-cell antigen recognition/activation of CD4.
- Antigen Presentation:
Professional APCs (e.g., dendritic cells, macrophages, or B cells) ingest and process extracellular antigens. - Processed antigens are presented on MHC class II molecules.
- The TCR on a naïve CD4+ T cell binds to the antigen-MHC II complex.
- The CD4 co-receptor stabilizes this interaction.
- Co-Stimulation:
- CD28 on the T cell binds to B7 on the APC, providing the second activation signal.
Cytokine Signaling:
- APCs secrete cytokines (e.g., IL-12, IL-4, IL-6), influencing the differentiation of CD4+ T cells into specific helper subsets:
- Th1 cells: Promote cell-mediated immunity (e.g., activate macrophages and CD8+ T cells).
- Th2 cells: Enhance humoral immunity (e.g., stimulate B cell antibody production).
- Th17 cells: Recruit neutrophils for extracellular pathogen defence.
- Effector Functions:
Activated CD4+ T cells secrete cytokines like IFN-γ (Th1), IL-4 (Th2), or IL-17 (Th17) to orchestrate the immune response.
what do TCRs bind to and what occurs as a result?
- antigens
- MHC I and II
- Trigger activation of T cells.
- CD4+ T cells secrete cytokines to regulate the immune response.
- CD8+ T cells kill infected or abnormal cells.
what do BCRs bind to and what occurs as a result?
- BCRs bind to native antigens in their unprocessed, three-dimensional form. These can include:
- Proteins (e.g., viral capsids, bacterial toxins).
- Carbohydrates (e.g., polysaccharides on bacterial surfaces).
- Lipids or nucleic acids (though less commonly).
Unlike TCRs, BCRs do not require antigens to be presented by MHC molecules.
- Trigger activation of B cells.
- Activated B cells differentiate into plasma cells that secrete antibodies targeting the specific antigen.
name the different types of CD4+ T helper cells, state their individual roles, what cytokines they release and what they provide defence against.
Role: Orchestrators of the immune response by activating and directing other immune cells.
Mechanism: Recognize antigens presented by MHC Class II on professional antigen-presenting cells (APCs) like dendritic cells, macrophages, or B cells.
Subtypes:
Th1 Cells:
- Promote cell-mediated immunity.
- Activate macrophages and CD8+ T cells.
- Key cytokines: IFN-γ, IL-2.
- Defense against: Intracellular pathogens (e.g., viruses, some bacteria).
Th2 Cells:
- Promote humoral immunity (B cell activation and antibody production).
- Key cytokines: IL-4, IL-5, IL-13.
- Defense against: Extracellular pathogens (e.g., helminths, allergens).
Th17 Cells:
- Drive inflammation and recruit neutrophils.
- Key cytokines: IL-17, IL-22.
- Defense against: Extracellular bacteria and fungi.
T Follicular Helper Cells (Tfh):
- Assist B cells in germinal centers to produce high-affinity antibodies.
- Key cytokines: IL-21, IL-4.
name the role, mechanism and what they defend against for CD8+ cells.
Role: Kill infected, cancerous, or damaged cells directly.
Mechanism: Recognize antigens presented by MHC Class I on any nucleated cell.
Effector Mechanisms:
Release perforin (forms pores in the target cell) and granzymes (trigger apoptosis).
Secrete IFN-γ to inhibit viral replication.
Defense Against: Intracellular pathogens (e.g., viruses) and tumor cells.
outline the different types, role and mechanism for regulatory T cells.
Role: Suppress and regulate immune responses to prevent autoimmunity and excessive inflammation.
Mechanism:
Recognize antigens presented on MHC Class II.
Secrete inhibitory cytokines: IL-10, TGF-β.
Directly suppress effector T cells and APCs.
Types:
Natural Tregs (nTregs): Develop in the thymus.
Induced Tregs (iTregs): Differentiate in the periphery.
outline the role and the different types of memory T-cells.
Role: Provide long-lasting immunity by remembering specific pathogens.
Types:
- Central Memory T Cells (Tcm): Reside in secondary lymphoid tissues and respond quickly upon re-exposure.
- Effector Memory T Cells (Tem): Circulate in peripheral tissues and provide immediate effector responses.
- Tissue-Resident Memory T Cells (Trm): Remain in tissues where the infection occurred.
outline the role and mechanism of gamma delta T cells and what they defend against.
Role: Act as a bridge between innate and adaptive immunity.
Mechanism:
Recognize antigens without the need for MHC presentation.
Produce inflammatory cytokines and exhibit cytotoxic activity.
Defense Against: Mucosal pathogens and stress-induced damage.
outline the role and mechanism of natural killer T cells and what they defend against.
Role: Share features of both T cells and natural killer (NK) cells.
Mechanism:
Recognize lipid antigens presented by CD1d molecules (non-classical MHC).
Produce cytokines like IFN-γ and IL-4.
Defense Against: Tumors and pathogens, particularly in mucosal tissues.
outline what is clonal selection and expansion.
Once activated, the T cell undergoes clonal selection and clonal expansion.
Clonal Selection:
The activated T cell proliferates, producing a clone of identical cells that are specific to the same antigen.
Clonal Expansion:
The selected T cells expand rapidly, forming a large population of T cells that can recognize the same pathogen.
These cloned T cells differentiate into either effector T cells or memory T cells.
