Transcript
Introduction to the immune system
Innate immunitythe “front line” of defensenon specific
Acquired immunitymechanisms- antigen specificityimmunological memoryprinciples of vaccination
Important features of the immune system
Must be able to distinguish foreign antigens fromself antigens (what is an antigen?)
Must have memory (responds slowly to firstexposure, but more rapidly to subsequentexposures TO THE SAME ANTIGEN)
What does the immune system actually do?
Phagocytes- kill and remove foreign ordamaged cells
Antibodies- “tag” invading cells or viruses for destruction
Cytotoxic cells- killed altered cells
Regulate the immune response
What/where is the immune system?
Barriers
Circulating blood cells
Tissue-fixed cells
Lymphatic system
p. 375, physical barriers to infection
p. 377, origin of lymphoid cells
Cells with immune function (p. 378)GranulocytesNeutrophils
most common leukocyte (50-70%)most potent phagocyte
Eosinophils (2-4%)probably phagocyticinvolved in allergic responses, parasitic infections
Basophils (0-1%)mostly found in tissues (mast cells)release inflammatory molecules
Agranulocytes
Monocytes (5-10%)more common in tissues
In tissues:macrophages- phagocytes; help regulateimmune response (“antigen presenting cells”)
dendritic cells- present antigen to lymphocytes
Lymphocytes (20-40%)B cells- make antibodiesT cells- some are cytotoxic, some are regulatory
Where are the lymphoid cells?
In the blood
In the tissues
In the lymphoid system
Can be recruited to site of injury or infection
p. 396, the lymphoid system
The lymphoid system parallels the circulatorysystem
Primary lymphoid organs- where lymphoid cellsdevelopbone marrow (ALL blood cells)
thymus- T cells mature there (become cytotoxic or helper T cells) and thencirculate
Secondary lymphoid organsPurpose: to trap antigen and present it to lymphocytesMost lymphocytes actually reside in these tissues
Lymph nodes- “filter” antigen from lymph
Spleen- “filters” antigen from blood
Lymphoid tissue in mucosa, gut and skin
Innate defenses
If they are “non-specific” how are they actually activated-appropriately??
Barriersskinantimicrobial chemicals
lysozyme (in tears and salivastomach acidoxygen metabolites
normal flora (“healthy competition”)
If barrier is breached- then what?
Pattern recognition- something is perceived asabnormal
Damaged tissue
Structures associated with bacteria (peptidoglycan,LPS, etc.)toll-like receptors on phagocytes, endothelialcells- some recognizes viruses, tooCell is then activated in response
Toll-like receptors, p. 381
Complement proteins- circulate in blood
Are normally inactive, but become active when binding to antigen, or antigen-antibody complexes
What happens next?
A series of reactions, resulting in:destruction of antigeninflammationenhanced phagocytosis of antigen
Complement system, p. 382
Phagocytosis; how do the cells know whence toengulf?
detectors of microbes and/or damaged cells(pattern recognition)
response to cytokines (produced by damagedcells and other immune cells
complement receptors
What happens in phagocytosis?
Process of phagocytosis, p. 384
Neutrophils are more potent killers, but die quickly
Macrophages can present antigen; amplifyimmune responsecan prolong activity by regenerating lysosomes
Both contribute to inflammatory response toinfection and/or damage
What is the inflammatory process?
What triggers the inflammatory process?
What are the outcomes of inflammation?
What is apoptosis, and how does it preventinflammation?
Inflammatory process, p. 387
Inflammation is triggered by infection or injuryPurpose: to contain damage (and response)
repair damage
“Cardinal signs of inflammation”:swelling, redness, heat, pain
Why swelling?
Chemical signals are released by damaged tissue
Neutrophils, monocytes recruited to the site andenter tissuesfluid enters tissues, too
Why redness?
Chemicals promote vasodilation Blood vessel walls relax; more blood (and
therefore more blood cells) can bebrought to the region
Why heat?Chemicals raise temperature at the spot(pyrogens)Increased temperature kills microbes
phagocytes are more activemore cells are formed
Effect can be systemic (fever)
Why pain?
Chemicals effect free nerve endings (painreceptors)Pain inhibits mobility; can help localizedamage
Inflammation can cause a lot of “bystanderdamage”
Ideally, damaged is confined to the site of injury
Some sites are more sensitive to damage thanothers
Damage can be systemic (septic shock, dueto blood infections: loss of blood volume,tissue damage, excess clot formation
Not all cell death causes inflammation
Apoptosis: programmed cell death
Under genetic control
(In immune response a large number of cells areformed to fight the infection- what happens tothem after the infection is cleared?)
Summary
Innate defense consists of barriers, phagocytesurveillance, and mechanisms to detectinfection or damage
Inflammation is the first line response to infection
Lymphocytes may be activated during this processwhich will respond more rapidly and inten-sively to subsequent infections