Non-specific immunity Flashcards
What defines and constitutes the first line of defense?
1st line - chemical and mechanical barriers
- surface membrane barriers
- skin and mucous membranes and their secretions
mechanical
- stratified squamous ET (stratum corneum) of skin
- mucous membranes lining body cavity
Chemical
- acidity of skin secretions
- HCl and digestive enzymes of stomach/small intestine
- bactericidal enzymes of saliva and tears
- mucous traps of digestive and respiratory tracts
What are some components of the 2nd line of defense?
phagocytosis, natural killer cells, fever, inflammatory response
how does phagocytosis contribute to nonspecific immunity? what cells are responsible?
macrophages and neutrophils and eosinophils
- none require specific receptors on surface
- ingest any foreign cells
intracellular digestion
release of free radicals, defenses
opsonization - coating of complement protein and antibodies to enable phagocytosis of foreign cells/particles
how do natural killer cells contribute to nonspecific immunity? what do they develop from? what do they have receptors for?
develops from same line as T ells - non specific form of lymphocyte
- does have receptors for constant region of antibody, but does not require recognition
kills cancer cells/virus infected cell before activation of immune system
- similar to killer T cell: releases perforin and granzyme B
- perforin pokes holes in cell membrane, granzyme ruptures inside of the cell
how do fevers contribute to nonspecific immunity? what organ is in charge of regulation body temperature?
leukocytes and macrophages release pyrogens
- pyrogens - reset body temperature by causing hypothalamus to increase temperature
increased temperature inactivates bacterial enzymes
- sequesters ion and zinc needed by bacterial enzymes into liver and spleen
- increases metabolic rate of cells
how does the inflammatory response contribute to nonspecific immunity?
inflammation brings increased number of phagocytic ells and plasma proteins to the invaded area
- help isolate, destroy or inactivate the foreign cells/virues
- remove debris
- prepare for healing or repair
begins with flood of cytokines (inflammatory chemicals) released into the ECF by injured tissue
- 5HT and histamine in crease permeability
describe the role of the following chemicals in the inflammatory response: prostaglandins, plasma bradykinin, histamine and heparin
what affect do steroids have on inflammation?
prostaglandins - vasodilation, increase capillary permeability
plasma bradykinin - vasodilation, increase permeability
histamine - vasodilation and increased permeability
heparin - prevents clotting and injury site
steroids decrease inflammatory response and decrease healing
what if interferon? what releases it? what are its functions?
anti-microbial protein synthesized in cells that are infected by a virus
- also released by activated lymphocytes, macrophages
function - simulate neighboring cells to make antiviral proteins which prevent replication of the virus
- does not protect infected cells
- autocrine/paracrine: travels short distance to warn other cells
- antiviral effects: activation of macrophages and mobilization of NK
what is complement? what are the two pathways?
anti-microbial proteins - similar to clotting proteins
- produced by liver
- activated in cascade
classical pathway - involves activation by Fc fragment of antibody
- rapid - linked to immune system (specific)
alternate pathway - does not need antibody (nonspecific)
- triggered by complement activation
- triggered by polysaccharides of bacterial coat
what are the first steps of the classical and alternative pathway? describe the following steps
classical - antibody exposure activates C3
alternate - complement/sugar interaction activates C3
- C3b binds to target cell surface
- triggers insertion of membrane attack complexes (MAC)
4, form and stabilizes opening in target cell membrane - interferes with target cells ability to release Ca
- provides binding sites for macrophages/neutrophils
- stimulates basophils/mast cells to release histamine
- attracts neutrophils
Describe the 3 ways complement destroys pathogens: enhanced inflammation, opsonization, cytolysis
enhanced inflammation - complement C3a stimulates mast cells/basophils to release inflammatory chemicals
opsonization - complement C3b makes bacteria easier to phagocytose by coating surface
- serve as binding sites for macrophages and neutrophils
cytolysis - complement C3b leads to rupture of target cells
- triggers insertion of MAC proteins which allows cytoplasm to leak out
Describe what C3a/b and C5a/b do in the complement pathway
C3/5a - triggers mast cells/basophils to release histamine and increase inflammatory response
C3b - binds to surface of bacteria for opsonization - increases changes of phagocytosis
- OR can bind to C5 and split it
C5b - binds with C6-9 and makes donut like opening - MAC
- causes cytolysis
describe specificity and memory of the specific immune response
specificity - immunity directed against particular pathogen
- immune system has ability to recognize particular substance
memory - ability of immune system to recognize the repetition of previous event
- provides more rapid response
what is an antigen? define the following: hapten, antigenic determinant, antigenic receptor, and epitope
antigen - substance that stimulated the immune response
- typically large molecule - protein, polysaccharide, lipids
hapten - molecules of low molecular weight that are too small to be antigenic on their own, but can become antigenic by binding larger molecule
antigenic determinant - immunogenic site on the antigen that antibodies or T lymphocytes can bind
antigenic receptor - molecules on the surface of B/T lymphocytes which recognize and combine with particular antigenic determinants
epitope - specific sequence of AA/polysaccharides on antigen surface that would fit variable component of an antibody
do T cells make antibodies
no, but they have receptors on their surface that function similarly to antigens
- receptor specific to antigen epitope
- can get multiple responses to same antigen due to different epitopes on surface
what is a polyclonal response? how is this possible?
different components react to different epitopes on the same antigen
most naturally occurring antigens have many sites that:
- activate several different lymphocyte populations
- bind different kinds of antibodies
describe the role of the t lymphocyte in the immune system
originates in red bone marrow, mature and multiply in the thymus
- each cell recognizes only one antigenic determinant
- selection occurs in thymus
competent lymphocytes reside in diffuse lymphatic tissue, spleen, lymphatic nodules, and in the paricortical and medullary areas of lymph nodes
describe the role of B lymphocytes in the immune system. what happens when they are activated?
originate and mature in red bone marrow
- one lymphocyte produces antibodies which recognize only one antigen
reside in diffuse lymphatic tissue, spleen, germinal centers of lymphatic nodules
when activated - increase ribosomal ER and golgi apparatus
- increases amount of cytoplasm
describe the role of macrophages in the immune system. what do they arise from?
arise from monocytes in the blood
secrete chemicals which activate T/B cells
T cells secrete chemicals that activate
act as antigen presenting cella
reside in loose CT, lymph node sinuses, lung, liver sinusoids
what is an APC? what dose a helper T cell do?
antigen presenting cell - must be phagocytic
- lysosome breaks down antigen into protein components and present them on the surface
T helper cells - undergoes cellular changes that recognize specific epitope of specific antigen
- cellular changes allow T helper cells to release molecules that activate T/B cells - causes them to multiply
what is an MHC class I molecule? what is its function? what is the purpose of TAP channels on ER
found on any nucleated cell in the body
function - present antigens produced internally on the external surface of plasma membrane - endogenous proteins
- MHC I /antigen complex can bind to a T cell receptor to activate the T cell
- T cell can destroy the cell demonstrating MHC I/antigen complex
TAP channel - allows molecules into lumen of ER
- binding site of MHC I on inside of lumen, need to let molecule in
- TAP: transporter associated antigen processing
once the MHCI receptor/antigen is presented, what happens next?
T killer (cytotoxic) cells interacts with MHC I
- CD8: specific binding site on T cytotoxic that recognized MHCI
- intermolecular binding - activates T cells, stabilizes activity
what is the MHC class II molecule? What is its function>
found only on antigen-presenting cells - exogenous antigen
- macrophages, B lymphocytes, monocytes, dendritic cells
engulf foreign antigen - binds with protease enzymes to degrade antigen into antigenic components
- vesicle binds with golgi or ER
MHCII on the golgi or ER leaves and presents antigen
What happens after MHCII receptor/antigen is presented?
T helper interacts with MHCII
- CD4: specific binding site on T helper that interacts with MHCII
- intermolecular binding - activates T cells, stabilizes activity
