Adaptive Immunity Flashcards
Adaptive (specific) immunity:
3rd line of defense
•Adaptive immunity directed against specific pathogen
•Prior exposure necessary: acquired immunity
- Has memory: “primed” after antigen 1st encounter- faster, stronger response 2nd time
•Self- tolerance: does not target self-antigens
•Systemic: not restricted to initial infection site
• Lymphocyte populations: produced in red bone marrow, mature in red bone marrow or thymus
- T-cells and B cells
Antigens:
•unique glycoproteins found on all cells/biological molecules
- Foreign (non-self) antigens-activate adaptive immunity and cause immune response
- Self-antigens- Not foreign to you (might be antigenic to others, blood transfusions?)
Major histocompatibility complex
(MHC):
•proteins in cell membranes,
“docking stations”
- Class I MHCs: on all nucleated cells always
- Class II MHCs: only on phagocytic antigen presenting cells (macrophages, dendritic cells,
B cells) during immune response
T cells (cell mediated immunity)
• Kills abnormal cells: cancer, virus-infected etc., helps others destroy .
•T cells can not bind free floating antigen, must have the antigen processed and presented to them on another cell’s surface
• Some T cells “help” B cells
B cells (humoral or antibody mediated immunity)
Produces Abs against antigens in blood, lymph - Abs bind antigens, cause elimination of antigen
Maturation of lymphs
• Lymphocytes become “educated” immunocompetent and self tolerant
- T cells in thymus, B cells in bone marrow
- Produce lymphocytes that are immunocompetent (trained to recognize foreign antigen as part of immune response), self tolerant (not self-reactive!) but… still naïve (haven’t encountered real antigen yet)
• T cells become:
- CD4* helper T cells or CD8+ cytotoxic T cells
-Migrate to secondary lymphatic structures- ready for Ag.
T Cell receptors interact with MHCS
T cells have receptors (TCR) -must interact with MHC and bind specific antigens before T cell becomes activated
Antigen presentation pt. 1
•MHC I (on all nucleated cells) and MHC II (antigen presenting cells only: macrophages, dendritic cells, B cells) used to present
•Healthy cells incorporate normal self antigens into MHC I = no response
•Unhealthy cell incorporates foreign antigens into MHC I = immune response
Antigen presentation pt. 2
• T cells must have antigen presented so they can “see” it
•Viral infected cell, abnormal cancerous cell: MHC I molecules will have bound foreign antigen (BUT! endogenous antigen made in cell)
•CD8* Cytotoxic T cells “see” antigen, bind, directly destroy cell
CD8+ Cytotoxic T cell activation
• CD8+ cytotoxic T cell receptors bind
Class I MHC proteins with endogenous foreign Ag on abnormal cell (virus infected, cancerous)
• CD8+ T cell activated (helper CD4* T cells cytokine helps we will see!), divides, producing both:
- Cytotoxic T cells: roam, seek and directly attack and destroy abnormal cells with target antigen = “cell-mediated” immunity
- Memory cytotoxic T cells: remain inactive, not mature:
• See antigen a second time- quickly become cytotoxic
Cytotoxic CD8+ T cell effects
•Cell-mediated function of activated cytotoxic T cells
• Function somewhat similar to NK cells
• Perforin: increase cell’s permeability and allows entry of:
- Granzymes: enter and trigger death program causing cell death
- Abnormal host cell is sacrificed for greater good of host
• Different than NK cells:
Cvtotoxic T cells are specific!
Antigen presenting cells (APCs):
also display MHC II (in addition to MHC I!)
- Macrophages, Dendritic cells (i.e. Langerhans cells in skin epidermis), B cells present to T cells in lymphatic structure. “professional” APCs!!
-MHC II presents antigen part of substances phagocytosed by APC (So!-exogenous antigen) - activate CD 4+ “helper” T cells
Helper CD4+ T cell activation
• Inactive CD4+T cell receptors recognize
APC Class I MHC with specific foreign Ag-> binds, releases cytokines- DO NOT DIRECTLY KILL!
• CD4+ Helper T cell activation, divides,
produces 2 types CD4+ cells:
- Active Th cells that release cytokines but don’t directly kill: purpose?
• Stimulate helper T cell divisions
• ^ activation of CD8* cytotoxic T cells
• Increase macrophage phagocytosis
• Activate B cells!! (later)
- Memory T cells: inactive
• Involved in all branches of immunitv: innate and adaptive (cell-mediated and antibody mediated) immunity
B cell activation
• Antibody-mediated (humoral)
immunity
• B cell recognizes specific free Ag outside of cell-›BCR (B cell receptor) -> engulf -> processes
•Presents Ag on MHC Il to helper T
cells = antigen presentation right?
- Helper T cells binds and helps fully activate B cells with cvtokines!
•Following full activation- B cell divides clonal selection) and produces
- Plasma cells: short-lived B cells that secrete antibod
• Antibody: immunoglobulin proteins that bind to that specific Ag - Memory B cells: long-lived reserve, MANY!
• With 2nd exposure- rapidly become antibody secreting plasma cells
So what about those antibodies binding to antigens?
• Antibodies: Immunoglobulin (Ig) protein made by plasma cells (antibody producing B cell line) in blood/lymph against specific antigen
•Plasma cells short-lived, but make hundreds of millions of Ab
• Ab binding to antigen (Ag) forms Ab-Ag complex -causes elimination of Ag
