blood and immune system Flashcards
Innate immune system
Immune system you are born with
- first line of defence so is rapid
-non specific
-barriers to keep harmful materials from the body.
Aquired immune system
-developed when your body is exposed to an antigen
-antigen specific
-capacity for memory
-rapid and specific response
Physical barriers
-epithelial layers (outer surface of the body,organ and blood vessels e.g. skin )
-hair
-fluid
-mucus
Respiratory epithelia
- cells are ciliated. Mucus traps the pathogen and Cilla beats it out of the lungs to be coughed up or swallowed
Cellular barriers
-activates when there is a breach to the physical barriers
-white blood cells collect at the site of infection
-phagocytosis = engulf and degrade pathogens. Under gone by neutrophils (short lived), macrophages,mast cells,dendritic cells (long-lived)
natural killer cells
- Kill virally infected cells
-can detect and control cancer cells
Humoral responses
Secreted macromolecules that protect you
- cytokines _ proteins that alter the behaviour of other cells
-chemokines- proteins that attract other cells
Complement
- Blood plasma proteins that defend againstinfection
- contact with pathogen causes an activating protease cascade
- enhance the ability of antibodies and phagocytes Cells
Interferons (IFN)
- innate response to viral infections
-release IFN proteins which stimulates neighbouring uninflected cells to become antiviral
Acquired immune defences
- Cellular = cytotoxic t- cells, T-helper cells and B lymohocytes
-Acellular =antibodies and cytokines
Roles of t and B lymphocytes
-T-cells directly attack infected or abnormal cells
-cytotoxic T cells recognise and kill virus-infected cells,cancer cells and cells that display abnormal antigens on their surface
- B cells = produce antibodies which neutralise pathogens
cytokines
-signalling molecules
-aid cell-cell communication and stimulate the movement of cells to the site
connectivity of the immune system
-once the pathogen enters the barriers the innate responses stimulate the adaptive immune system
-adaptive responses stimulate innate
pathogen-associated molecular patterns (PAMPS)
- repeating molecules common in pathogens that are absent from human cells
-Recognised by receptors called PAMP recognition receptors (PRRs)
Toll-like receptors
-type of PRRs
-on the cell surface and binds to bacterial peptidoglycan
-som bind to DNA or RNA
-binding of peptidoglycan activates a cell cascade resulting in an immune response
Damage associated molecular patterns (DAMPs)
-releases signals by stressed, injured, or dying cells.
-can a activate innate or adaptive immune cells to cause a response
-can activate inflammation
four concepts in immune recognition
- Innate immune response:
- Can recognise generic features of pathogens (PAMPs)
- Can recognise danger signals from non-apoptotic cell death (DAMPs)
- Acquired immune response:
- Can learn to recognise specific pathogens (adaptive immunity)
- Can ignore human molecules (self-tolerance)
inflammation causes
-injury
-autoimmune
-pathogen
-chemical/toxins
mechanism of inflammation
-infection/wound triggers the host response
-host responses include immune cell recruitment, vascular changes(histamines), tissue remodelling
example of mechanisms which causes symptoms of inflammation
-capillary widening=increased blood flow=heat
-increased permeability of cells-fluid releases into tissues-redness/swelling
-attraction of leukocytes(white blood cells
)= extravasation of white blood cells to the site of injury=tenderness
-systemic response= fever and proliferation of white blood cells=pain
vascular changes
vasodilation= increases of oxugen passing through and waste product removal and a decrease in blood pressure
stimuli for vasodilation
- Histamine – released by tissue
resident mast cells or basophils - Prostaglandins and leukotrienes –
released by neutrophils and mast
cells - Nitric oxide as a result of clotting
pathways - Protein products of complement
activation
leukocyte migaration
- The passage of leukocytes in and out of blood vessels, lymphatic vessels
and tissues. leukocytes travel through the blood. endothelium cells release signals to tell the leukocytes that there is a site of damage so leukocytes latch onto endothelium receptors. when they travel through small capillaries they begin rolling/crawling and then undergo paracellular and transcellular transmigration to pass through the cell and migrate into the tissue
-migration is due to the chemotactic gradient
immune deficiency
- More frequent infections
- More damage from each infection
- Damage from unbalanced immune
response unrelated to infection
(inflammation, allergy,
autoimmunity) - Increased risk of cancer
example of disorder immune responses
-arthritis,lupus,aids,leukemia.asthma,allergys
the hygiene hypothesis
-it explains the increasing prevalence of allergic and autoimmune diseases in industrialized countries.
-suggests that the reduction in exposure to infectious agents and microorganisms in early life, due to improved hygiene practices and sanitation, leads to an inadequately primed immune system
lymphoid tissue
-where the blood and the lymph meet
B and T helper cells
-they have antigen receptors on the cell surface. each cell has one type of receptor and each receptor is specific for a single antigen
lymphoid circulation
-non-lymphoid cells pass through in blood vessels
-lymphoid cells move from blood to lymph node through high-endocytic venules
-lymphatic cells are concentrated in the endocytic venules and exit through the lymphatic vessels
cells in lymphoid follicles
-dendritic cells arrive in the lymph-loaded with antigens to present to B and T cells
- B and T cells arrive from the blood, each with its receptors waiting to be activated by antigens on the dendric cells
-B and T cells get activated
-activated T cell interacts with activated B cell (cytokines) to stimulate it
-B cells make antibodies
germinal centre formation
-once the B cells are activated prior via dendric cells
-Some of the activated B cells migrate to the follicles of lymphoid organs and form germinal centers.
-Within germinal centers, B cells undergo rapid proliferation
-B cells undergo mutuations which generates a diverse pool of B cells with slightly different antibody receptors
-B cells with antibody receptors that bind more strongly to the antigen presented by follicular dendritic cells are more likely to survive and proliferate further
- results in the production of antibodies with increased specificity and effectiveness against the antigen.
- Some of the B cells differentiate into long-lived plasma cells, which produce large quantities of antibodies. Others become memory B cells, providing long-term immunity against future encounters with the same antigen.
clonality
-lymphocytes that was activated proliferates to form clones with the same receptor specificity
clonal selection
-Naive lymphocytes encounter specific antigens from pathogens.
-When a lymphocyte’s receptor matches the antigen, it becomes activated.
-The activated lymphocyte undergoes rapid division, creating many copies of itself (clones).
-Some of the cloned B cells differentiate into plasmacells which produce antibodies and some memory cells
primary immune response
-the initial reaction of the immune system to a specific antigen, such as a pathogen or foreign substance, that the body encounters for the first time
-starts within antigen recognition
-Antigen-presenting cells present antigens to helper T cells
-Activated helper T cells release cytokines that help regulate and coordinate the immune response.
- Activated B cells then differentiate into plasma cells, which produce and release antibodies specific to the antigen.
-developed memory cells
antigen structure
-similar to an antibody structure with two identical heavy chain and two identical light chains
-has a constant and variable region
-variability in the proteins Complementarity determining regions controls how the protein folds
how is the diversity of antigens made?
-combinational diversity= com
why is a mechanism of self-tolerance needed?
-self-recognising cells could be harmful if it underwent clonal expansion
-a mechanism to remove cell-recognising self-antigens from the repertoire before clonal expansion is established
