Lymphatic System Flashcards
immunity
ability to resist damage from foreign substances (microorganisms, harmful chemicals)
- innate or non specific resistance
- adaptive or specific immunity
innate immunity or non-specific
Generalized (“me antigen”) and will defend against all foreign invaders.
Primary immune response
Mechanical: prevent entry or remove microbes
Chemical: promote phagocytosis and inflammation
Adaptive or specific immunity
Adapted to fight specific targets is the secondary immune response
Specificity: recognize particular substances
Memory: (t cells) remember previous encounters with a particular substance, and respond rapidly
complement
group of 20 proteins circulate in blood and become activated in a cascade event
- classical pathway
- alternate pathway
activated complement proteins
- form membrane attack complex (MAC): make channel thru PM
- attach to surface of cells to phagocytize
- attract immune system components to promote inflammation (neutrophils and basophils)
classical pathway
(part of adaptive immunity)(complement)
- secondary immune response that requires antibodies to bind to antigens
- have helper T cells
alternative pathway
(innate immunity)(complement)
C3 binds with foreign substances to attract phagocytes
interferons
produced by infected cell and cause neighboring cells to produce antiviral proteins (paracrine)
neutrophils
A type of white blood cell that engulfs microbes by phagocytosis
- enter infected tissue first with phagocytes
- clean and eat; fast and motile
- 60% all WBC
macrophages
monocytes that have left bloodstream and enter tissues
- spleen, bone marrow, liver, lymph nodes
- large phagocytes
basophils and mast cells
-Promote inflammation when activated by innate or adaptive system
-Release histamine
-“somebody is here! Come get him!”
-Mast cells is basophil that is stationary and in CT
eosinophils
-Leave blood and enter tissues
-Reduce inflammation and break down chemicals made by basophils and mast cells
-Secrete enzymes that kill parasites
-Produce antihistamine
-React to call of basophils/mast cells
natural killer cells
a type of lymphocyte that attacks tumor cells and virus-infected cells
- recognize class of cells, not specific ones
inflammatory response: Local vs Systemic
Local: confined to a specific area. Symptoms are redness, heat, swelling, pain, loss of function
Systemic: occurs in many parts of the body. additional symptoms:
increase neutrophil # by bone marrow, fever (pyrogens), increase vascular permeability (histamine). Large volume of plasma in Interstitial space = shock
Inflammatory Response
Bacteria enter tissue
Tissue damage occur
Chemical mediators released (increase blood flow, chemotaxis, increase vascular permeability)
Increase numbers of WBC and chemical mediators at site of tissue damage
Bacterial are contained, destroyed and phagocytized
Bacteria gone> tissue repair OR bacteria remain > additional chem mediators activated > chemical mediators released (positive feedback loop = death)
self antigen
(aka me antigen)
body’s own antigen
- used as marker for adaptive immunity to differentiate btwn self and nonself
haptens
antigens too small to provoke immune responses; attach to carrier molecules to make an adaptive immune response
humoral immunity / Antibody-mediated
humoral (fluid); antibody-mediated (extracellular attack)
B cells and antibodies than can only attack extracellular things
Cell-mediated
T cells in adaptive immunity
positive selection of lymphocytes
-Ensure survival of lymphocyte react against antigens then proliferate/clone
-Find lymphocyte that react against antigen and will kill it
Aren’t killing so kill
negative selection of lymphocytes
-Eliminate clones of lymphocytes react against self-antigens
-Kill anything, even me antigens
-Comes after positive selection and remove those that don’t recognize the me antigens
killing things that are killing the wrong things
tolerance
state of unresponsiveness of lymphocytes to specific antigen and usually to self antigen (one’s own cells) - wont kill you
-Negative selection selects for tolerance
B and T cells
- types of lymphocytes
- both originate in bone marrow
- B cells mature in bone marrow; T cells mature in thymus (primary lymphatic organs)
- secondary lymphatic organs/tissues are where B and T cells go to work (lymphatic tissues, nodes, nodules, etc)
activation of lymphocytes
- Lymphocytes must be able to recognize the antigen
- After recognition, lymphocytes must increase in number to effectively destroy antigen
antigenic determinants
specific regions of a given antigen recognized by a lymphocyte. On the antigen
-antigenic receptors: surface of lymphocyte combine with antigen directly. On the lymphocyte
-activation with glycoproteins: Major histocompatibility complex (MHC) molecules attached to PM and variable region can bind to foreign and self antigens
Major Histocompatibility Complex (MHC): Class I
-On nucleated cells surface
-Cell that has become infected and displayed antigen on outside of it
-Antigen protein broken into fragments
-Broken fragments go to ER and join w MHC I molecules
-self antigen and foreign antigen displayed on cell surface
-Both foreign antigen and self antigen marked by MHC 1 molecules and are both recognized by T cell or macrophage to kill it (cell that has to die bc its infected)
Major Histocompatibility Complex (MHC): Class II
Macrophage has consumed antigen as move around (antigen not enter cell but was eaten)
-Macrophage break it down and release MCH 2 molecules
-MCH 2 molecules attached to foreign antigen and displayed on PM
-Not “up for death” - nothing kills macrophage ; stimulates immune cells
Costimulation
helps to ensure that immune system doesn’t launch an attack in the absence of an enemy
- via cytokines
- via surface molecules
Costimulation by Cytokines
- Helper T cell approach macrophage with displayed antigen (MHC2) on PM
- helper T cell attaches to macrophage with T-cell receptor
- cytokines leave macrophage and attach to helper T-cell’s cytokine receptors
costimulation by surface molecules
- Helper T-cell extends receptor to attach to macrophage’s displayed foreign antigen (MHC2) on PM
-glycoprotein expands out of helper T cell and joins to antigen and can control and develop its own antigenic determinant (can recognize and build antigenic determinant of virus, important for T cells)
anergy
absence of the normal immune response to a particular antigen or allergen
- costimulation not take place
proliferation of lymphocytes
Cells from original clones must proliferate before antigen can be attacked effectively
1. Proliferation of Helper T cells (Cytokines)
2. Proliferation of B cells and effector T cells (surface)
-Helper T cell has downloaded information about antigen when join w macrophage (can teach soliders how to fight)
-Helper T cells release lympholukens and stimulate mytosis = new soliders
helper t cell proliferation
- Macrophage attached to helper T cell (MHC2)
- T cell release interluken 1 > interluken 2 > develop interluken 2 receptors
- Now make daughter cells (divide again or stimulate B or T cells)
proliferation of B cells
- B cell attach to helper T cell (MHC2) w CD4 anchoring; release interleukins into B cell
- unprocessed antigen go to B cell receptor to get eaten
- B cells can make daughter cells which make antibodies
lymphocyte inhibition
- Tolerance: state of unresponsive of lymphocytes to a specific antigen
Provoked by:
§ Deletion of self-reactive lymphocytes
§ Preventing activation of lymphocytes that encounter self antigens
§ Activation of suppressive T cells: cells that may produce suppressive cytokines or kill antigen-presenting cells
antibody-mediated immunity
Effective against extracellular antigens when they are outside cells
- variable region: combine w antigenic determinate of antigen (Change shape, antigen binding cite)
- constant region: tell what to bind to and when (directs antibody or its reaction)
Actions of antibodies
-Antigen can directly attach to antibody
-antigen can attach to many antibody
-Antigen attach to antibody to release inflammation, chemotaxis, lysis
-Antibody can be attached to mast cell and have antigen attach to make inflammation
-Antigen and antibody can attach to macrophage + consumed (constant region)
antibody production: Primary response
3-14 days (innate)
-B cell first activated by antigen then proliferate to make plasma cells and memory cells
-B cell eat antigen and come in contact w macrophage (first time) then have memory to make antibodies
Antibody production: Secondary Response
(adaptive) 8-24 hrs
-Memory cells divide rapidly to make plasma cells and additional memory cells (Faster and greater response)
-B and T cells are primed and ready (don’t have to go thru learning process) to go
cell-mediated immunity
- T cells fight things inside the cell
- either lyse cells (perforin) to kill or release cytokines (phagocytosis and inflammation)
- memory cells are made
proliferation of cytotoxic t cells
- cytotoxic T cell binds with target cell (MCH1) anchoring with CD8
- helper T cell releases interleukin2 into cytotoxic T cell
- cytotoxic T cell now make daughter cells (have that binding cite)
immune interactions
Antigen attaches to macrophages which presents it to helper T-cells
T-cell proliferates then daughter T-cell can instruct B-cell + T-cells to make antigenic binding cites
A) Daughter bind to B-cell produces antigen
B) T-cell bind to cells that show antigen to cytokines
C) both daughter B+T-cells responsible for adaptive immunity
Cycle continues til antigen all gone
acquired immunity
-immunization
-Active natural immunity: (vaccine shot)
-Active artificial immunity: (first breast feed)
-Passive artificial immunity: immune animal to non immune transfer)
ways to get acquired immunity
Natural /artificial > activate immunity > acquired adaptive immunity (memory B and T cells)
Natural/artificial> passive immunity > acquired adaptive immunity
natural: get antigens thru natural exposure
artificial: antigens deliberately introduced thru vaccine
