Additional Ch 21 The Immune System

Front 1

Mast cells vs. basophils, list the differences.

Back 1

Both have histamine and herapin, and react to allergens, Mast cells hang in CT, and basophils are mostly in blood

Front 2

Describe the chemical barrier of the cutaneous layer.

Back 2

Skin has a mantle acid which lowers the pH from 3-5, acidic because of lactic acid secreted from skin, and fatty acids

Front 3

Describe how the cutaneous layer protects the body as part of the innate immune system.

Back 3

Outer layer composed of keratin-A (tough protein), mantle acid.

Front 4

Describe the importance of TLRs.

Back 4

Toll-like receptors look for PAMPS (pathogen associated molecular patterns). TLRs are located on epithelial cells and macrophages. TLRs are part of the innate immune system.

Front 5

Describe natural killer cells function and structure.

Back 5

NKCs are large granular lymphocytes that engage in immune surveillance and detect and destroy malignant cells that lack correct MHC I, or have a coating of antibody on the cell. NKCs kill by lysis

Front 6

Describe lysis, and list which cells use this method.

Back 6

NKCs and CD8s latch on to cell, perforin and granzymes are released, perforin opens pores, granzymes enter via pores, degrade cellular contents, stimulating apoptosis

Front 7

Describe apoptosis.

Back 7

Programmed cell death

Front 8

What are the 4 signs of inflammation, and what causes them?

Back 8

Dilation of blood vessels makes the injured area appear red and feel warm, Leakage of plasma causes swelling, pain, and loss of function. Swelling, pain, redness, warmth

Front 9

What causes increased permeability and what does it have to do with inflammation?

Back 9

Mast cells release chemicals that cause blood vessels near the would to constrict, while their release of histamine induce vessels further from the wound to dilate.

Front 10

Describe PLAN?

Back 10

Antibodies work by precipitation, lysis (by complement), agglutination, and neutralization.

Front 11

Describe how complement works, and where it is produced.

Back 11

Complement is a group of about 20 plasma proteins produced by the liver that normally circulate in the blood in an inactive state. Activation unleashes chemical mediators that amplify virtually all aspects of the inflammatory process. Kills certain bacteria w/ lysis. Cascade that causes cell lysis, promotes phagocytosis, and enhances inflammation

Front 12

Describe MAC.

Back 12

Membrane attack complex as result of complement causing lytic events.

Front 13

Interferons.

Back 13

Cells like leukocytes and reticular epithelial cells secrete interferons that bind to receptors on neighboring cells and activate second messenger mechanisms that inhibit viral replication, and also activate NK cells and macrophages.

Front 14

Describe the benefits of fever.

Back 14

Fever causes liver to sequester iron and zinc (needed by bacteria to multiply), and increases metabolic rate of tissue cells quickening their repair process

Front 15

Describe endogenous pyrogens.

Back 15

The cytokines (such as interleukin 1) are a part of the innate immune system, produced by phagocytic cells, and cause the increase in the thermoregulatory set-point in the hypothalamus. Other examples of endogenous pyrogens are interleukin 6 (IL-6), and the tumor necrosis factor-alpha.

Front 16

Describe exogenous pyrogens.

Back 16

One model for the mechanism of fever caused by exogenous pyrogens includes LPS, which is a cell wall component of gram-negative bacteria. An immunological protein called lipopolysaccharide-binding protein (LBP) binds to LPS. The LBP–LPS complex then binds to the CD14 receptor of a nearby macrophage. This binding results in the synthesis and release of various endogenous cytokine factors, such as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. In other words, exogenous factors cause release of endogenous factors, which, in turn, activate the arachidonic acid pathway.

Front 17

Describe how prostaglandins affect the inflammatory response.

Back 17

Generated by enzymes of neutrophils, basophils, mast cells and others, sensitize blood vessels to effects of other inflammatory mediators, generate free radicals which cause inflammation and induce pain

Front 18

Describe antigens.

Back 18

Any molecule that triggers an immune response.

Front 19

Describe the difference between complete and incomplete antigens (also called?).

Back 19

Complete Ags exibit immunogenicity, and incomplete antigens or haptens aren't antigenic by themselves but can bind to a host macromolecule and be recognized as foreign (e.g. cosmetics, drugs, poison ivy, etc)

Front 20

What is an antigenic determinant, and what are they also known as?

Back 20

Antibodies bind to epitopes on antigen surface. Most Ags have several different epitopes, which means different Abs can bind to them.

Front 21

Where do B cells go to school?

Back 21

Bone marrow

Front 22

Where do T cells go to school?

Back 22

Thymus

Front 23

Name the different kind of B cells.

Back 23

B cell, memory B, plasma cell, APC

Front 24

Name the different kind of T cells.

Back 24

CD4, CD8, T-regs, APCs

Front 25

B cells key weapon?

Back 25

Abs

Front 26

T cells key weapon?

Back 26

CD 8

Front 27

B's favorite hood?

Back 27

Blood

Front 28

T's favorite hood?

Back 28

tissue, lymphatic tissue, lymph nodes

Front 29

B's key target?

Back 29

extracellular (blood, bacteria, virus)

Front 30

T's key target?

Back 30

Infected cells, CA cells, transplants

Front 31

What is immunocompetence?

Back 31

Immunocompetence is the ability of the body to produce a normal immune response (i.e., antibody production and/or cell-mediated immunity) following exposure to an antigen. Opposite of immunodeficiency.

Front 32

What is self tolerance?

Back 32

Natural or "self" tolerance. This is the failure (a good thing) to attack the body's own proteins and other antigens. If the immune system should respond to "self", an autoimmune disease may result.

Front 33

What are the APCs?

Back 33

Macs, dendritic cells, B cells.

Front 34

Active immunity?

Back 34

Self produced

Front 35

Passive immunity?

Back 35

given from mother or vaccine.

Front 36

IgG?

Back 36

From mother, most abundant antibody.

Front 37

IgE?

Back 37

Causes cells to release histamine.

Front 38

IgM

Back 38

Potent agglutinating agent.

Front 39

Ab structure.

Back 39

Y shape w/ 2 heavy chains, and 2 light chains.

Front 40

PLAN?

Back 40

How Abs work: precipitation, lysis (by complement), agglutination, and neutralization

Front 41

Cellular mediated immunity?

Back 41

Cellular immunity protects the body by:

1. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens;
2. activating macrophages and natural killer cells, enabling them to destroy intracellular pathogens; and
3. stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses.

Front 42

Prostaglandins?

Back 42

cause aggregation or disaggregation of platelets

Front 43

Leukootrienes?

Back 43

Leukotrienes are naturally produced eicosanoid lipid mediators, which may be responsible for the effects an inflammatory response. Leukotrienes use both autocrine signalling and paracrine signalling to regulate the body's response. Leukotrienes are produced in the body from arachidonic acid by the enzyme 5-lipoxygenase. Their production by the body is part of a complex response that usually includes the production of histamine.

Front 44

Kinins?

Back 44

The kinin-kallikrein system or simply kinin system is a poorly delineated system of blood proteins that plays a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types.