recognition of what is self and what is not self. Defense against foreign invaders
Immunity
Cells and organs
Cytokines
Complement
Antibodies
Components of the immune system
white blood cells
Leukocytes
neutrophils, basophils, eosinophils
Polymorphonuclear granulocytes (innate immunity)
B cells, T cells, NK cells
Lymphocytes (adaptive immunity)
Produced in bone marrow Phagocyte Releases chemicals involved in inflammation
Neutrophil
Produced in bone marrow Release factors involved in inflammation
Basophil
Produced in bone marrow Destroy multicellular parasites Participate in immediate hypersensitivity reactions
Eosinophil
NK, B, and T cells NK and B mature in bone marrow T cells mature in thymus Serve as essential recognition cells in specific/adaptive immune responses
Lymphocyte
Produced in bone marrow In tissues, differentiates into macrophages Phagocyte
Monocyte
derivatives of B cells, make antibody
Plasma cells
derivatives of monotyes, in tissues, phagocyte
Macrophages
antigen presenting cell (APC), present antigen to T cells
Dendritic cells
found in connective tissues- skin granulocytes, important in wound healing + inflammatory response
Mast cells
proteins capable of killing bacteria and viruses
Complement proteins
Messengers of the immune system, chemicals released by immune cells
Cytokines
Too few WBCs (AIDS)
Leukopenia
Too many WBCs (infection)
Leukocytosis
Bacterial infection
High neutrophils
Viral infection
High lymphocytes
Proteins released by immune cells to perform a specific function Allow immune cells to communicate with each other
Cytokines
General defense. Attack invader based on general properties. Involves phagocytes + complement Cells recognize lipids or carbs on invader cell
Innate responses
Body produces antibodies to specific antigen. Involves lymphocytes Cells and antibodies recognize proteins on invader cell
Adaptive responses
Hyperemia, chemotaxis, diapedesis, colony, phagocytosis, complement, attack complex, tissue repair
Steps of inflammation
Mast cells (tissue basophils) and damaged tissue cells release histamine (vasodilator) and other factors Increased capillary permeability: fluid and plasma proteins leak into tissue Area becomes red, swollen, warm
Hyperemia
Injured tissues release chemicals that draw phagocytes to area. Macrophages become more active, Collectively these form "pus"
Chemotaxis
neutrophils and phagocytes squeeze through endothelial cells to reach site of infection
Diapedesis
Stimulating factors released by damaged endothelial cells and macrophages to produce more WBCs
Colony
Substances called opsonins bind to proteins on microbe and adheres phagocyte to microbe Engulfs by endocytosis
Phagocytosis
Plasma proteins circulating in blood, activated by carbs on microbial membranes; undergo cascade reactions to become activated (30 proteins)
Complement
MAC, forms pores in microbial membrane Some cause vasodilation, inc. vessel permeability to protein, and chemotaxis C3b: complement proteins that acts as an opsonin (bind to antigens and mark them)
Attack complex
Fibroblasts divide and secrete collagen, angiogenesis occurs May be imperfect->scarring
Tissue repair
Antiviral cytokines Cell is infected by virus->secretes IFN
Interferons (IFNs)
Developing lymphocytes insert 1 type of receptor that will bind to a specific antigen into plasma membrane. Progeny called clones
Adaptive immune response stage 1
Binding of antigen causes lymphocyte activation/proliferation. Clonal expansion. Some carry out attack, some become memory cells.
Adaptive immune response stage 2
Effector lymphocytes carry out attack. Extra lymphocytes after attack is carried out die of apoptosis.
Adaptive immune response stage 3
Produce lymphocyte precursors/early stages Bone marrow and thymus
1st degree lymphoid tissues
Where immune cells and antigens meet. Where antigens activate the receptors on the lymphocytes. Lymph nodes, spleen, tonsils
2nd degree lymphoid tissues
Occur in clusters throughout body Channels (macrophages) and nodules (lymphocytes, antigens)
Lymph nodes
Like lymph nodes, but for circulating blood. large collections of lymphocytes, macrophages, and dendritic cells.
Spleen
In pharynx. Filled with lymphocytes, macrophages, and dendritic cells -> crypts open to pharynx.
Tonsils and adenoids
Cancer of lymph nodes
Lymphoma
When activated, differentiate into plasma cells -> secrete antibodies- travel all over body, bind to specific antigens and guide attack, act as opsonins
B cells
A protein that acts against a specific antigen, mediated responses: humoral responses
Antibody
General term for lymphocytes that are responsible for immunological memory and protective immunity, some plasma cells differentiate into memory cells
Memory cells
attack cells -> bk activated, enter blood, seek out targets
CD8+ T cells
helper cells, activated, secrete cytokines that help B and CD8 cells function (neither cells can function without CD4)
CD4+ T cells
B cell receptors
Immunoglobulins
Provide specific responses for bacteria
IgG and IgM
participate in allergic responses
IgE
in gastrointestinal, respiratory, and genitourinary tracts. Act locally. Antibodies in milk.
IgA
functions unclear.
IgD
Does not recognize "free" antigen. Must be "presented" by proteins on other cells
TCR
found on surface of all of body's cells, except RBCs. TCR of CD8+ T cells binds to MHC class I
MHC class I
only present on antigen presenting cells (APCs) TCR of CD4+ T cells binds to MHC class II
MHC class II
macrophages, B cells, and dendritic cells
APCs
Created in: 2nd lymphoid organs after cells meet antigen B cells live in body for decades T cells live 8-15 years Allows faster response, basis for vaccines
Memory B and T cells
Bind to opsonized (by Abs) viruses and cancer cells via Fc receptor Can recognize virally infected cells Forms an immune synapse
NK cells
Released by NK cell, pokes holes in target cell membrane
Perforin
Derived through the holes that kill the target cell.
Granzymes
infects and kills CD4+ T cells Causes AIDS
HIV
CD4+ T cells bind to the HIV virus via:CD4+ protein itself and a coreceptor HIV kills CD4+ T cells and causes apoptosis of uninfected CD4+ T cells, no effective cure No CD4+ T cells: B cells and CD8+ T cells can not function -> patient dies from infections + cancer
AIDS
rapidly replicating virus kills large numbers of CD4+T cells but they are replaced and numbers remain constant. No symptoms.
1-5 years HIV
Balance is lost, # of CD4+ T cells goes down. Remain asymptomatic until T cell numbers get very low
Next 5 years HIV
Immune response causes inflammation and damage to body itself. Antigens that cause allergy: Allergens (ragweed, pollen, poison ivy)
Allergy (hypersensitivity)
Themselves are harmless, inappropriate immune response causes damage
Allergens
No antibodies involved Pronounced secretion of cytokines by helper T cells activated by antigen Cytokines act as: Inflammatory mediators, takes several days to develop ex. Tuberculosis skin test
delayed hypersensitivity
Initial exposure leads to: IgE synthesis, some memory cells Re-exposure: antigen elicits a more powerful antibody response
immediate hypersensitivity
Composed of: Small quantities of living or dead microbes Memory cells are produced after exposure to antigen—creates rapid, effective response to future infection.
Vaccines
a substance that is combined with the antigen (killed or inactivated virus or microbe) to enhance immune response against it
Adjuvant
Body's own proteins act as antigens and immune system attacks them
Autoimmune disease
Cardiac Muscle
Intercalated discs, desmosomes, gap junctions, arranged in layers and surround hollow cavities, squeezing
Sympathetic innervation of heart
throughout heart, release primarily norepinephrine
Parasympathetic innervation of heart
mainly in atria, release ACh
Blood supply to heart
Coronary arteries—supply myocardium with nutrients
Conducting cells
in contact with cardiac muscle cells via gap junctions, these cells initiate the heartbeat and spread the AP through the heart
Parasympathetic heart rate
Slows rate R vagus nerve -> SA node: slows firing L vagus nerve -> AV node Act to lengthen time to threshold
Sympathetic heart rate
Speeds rate Branches of thoracic spinal nerves go to SA & AV nodes & to ventricles
Systole
ventricular contraction and blood ejection
Diastole
ventricular relaxation and blood filling
Isovolumetric ventricular contraction
AV valves, aortic and pulmonary valves are closed. Tension is building in the ventricles
Ventricular ejection
blood flows out of ventricle, pulmonary and aortic valves open
Stroke volume
Volume of blood ejected
Isovolumentric ventricular relaxation
all valves are closed, ventricle is relaxing. Atria are filling. Pressure builds in the atria
Ventricular filling
AV valves open and blood flows in, SL closed. 80% of blood flows into ventricle before the atria contract
Lub-Whistle-Dup
Stenotic, SL
Lub-Gurgle-Dup
Insufficient, AV
Lup-Dup-Whistle
Stenotic, AV
Lup-Dup-Gurgle
Insufficient, SL
Cardiac Output (CO)
The volume of blood each ventricle pumps multiplied by the # of beats/min
Beta-blockers
Slow down HR by blocking beta adrenergic receptors- norepinephrine can’t bind
Frank-Starling mechanism
ventricle contracts more forcefully when more blood enters during diastole Ventricle walls stretch when more fluid enters: More stretch=more forceful contraction