Introduction to Immunology

Question 1

Innate Immunity

Answer 1

Includes epithelial barriers, phagocytes, dendritic cells, complement, and NK cells. Respond to PAMPS (pathogen associated molecular patterns). Receptors are identical on all cells of the same lineage. Occurs first, from 0-12 hours after infection.

Question 2

Adaptive Immunity

Answer 2

Includes lymphocytes, which respond to specific antigens. Receptors are encoded by genes produced by somatic recombination of gene segments to increase diversity. This system is clonal, in that clones of lymphocytes with distinct specificities express different receptors. Occurs after innate immunity, from 1-5 days after infection.

Question 3

Humoral Immunity

Answer 3

Responds to extracellular microbes by sending B lymphocytes. Antibodies are created to block infections and eliminate microbes.

Question 4

Cell mediated immunity

Answer 4

Responds to phagocytosed microbes in macrophage and intracellular microbes (viruses) replicating in a cell. Helper T lymphocytes and Cytotoxic T lymphocytes eliminate the microbes and kill reservoirs of infection.

Question 5

Granulocytes

Answer 5

Include neutrophils and eosinophils.

Question 6

Effector functions of B Cells

Answer 6

Antibody generation: neutralization of microbe, phagocytosis, complement activation.

Question 7

Effector Functions of Helper T Cells

Answer 7

Activation of macrophages, increase inflammation, activate other T and B Cells

Question 8

Effector Functions of Cytotoxic T Cells

Answer 8

Killing of infected APC

Question 9

Where do lymphocytes come from?

Answer 9

Bone marrow (B cells), Thymus (T cells).

Question 10

Where to lymphocytes encounter immunogens?

Answer 10

In lymph nodes and mucosal/cutaneous lymphoid tissues.

Question 11

Organization of peripheral lymphoid organs

Answer 11

B cell areas and T cell areas are distinct.

Question 12

Mucosal immune tissue

Answer 12

Unique, has to balance responsiveness with recognition of commensal bacteria.

Question 13

Neutrophils

Answer 13

Increase most rapidly during infection. Short lived professional phagocytes. Also known as polymorphonuclear leukocytes. Marker of acute inflammation. Once they become engorged with bacteria, they die and make up pus.

Question 14

Monocytes/Macrophages

Answer 14

Longer lived than neutrophils. Phagocytose microbes, serve as antigen presenting cells. Activated by cytokines. Major bridge to adaptive immunity.

Question 15

How do phagocytes dispose of an ingested microbe?

Answer 15

Microbe binds to PAMP receptor, gets endocytosed in phagosome, fuses with lysosome. Can be killed by enzymes in lysosome or killed by ROI’s and NO.

Question 16

PAMP Receptors

Answer 16

Recognize pathogenic patterns, include TLR’s lectins, NOD-like receptors, RIG-like receptors. Can occur on cell membrane, in cytosol or in endosomes.

Question 17

TLR Signaling Cascade

Answer 17

Binding to TLR, recruitment of adaptor proteins, activation of transcription factors like NF-kappaB and IRFs (interferon regulatory factors). NFkB increases cytokine production to stimulate inflammation and adaptive immunity. IRFs produce interferons, which are anti-viral.

Question 18

NOD-like Receptors

Answer 18

Nucleotide Oligomerization Domain (NOD) like Receptors lead to the release of IL-1ß, which causes acute inflammation.

Question 19

Inflammatory Response characterized by…? How is it initiated?

Answer 19

Increased blood flow, increased vascular permeability, fever, pain. Initiated by microbe-phagocyte induced release of cytokines like TNF, IL-1 and chemokines. Also anaphylatoxins from complement, leukotrienes, prostagladins, etc.

Question 20

Sentinel Cells

Answer 20

Macrophases and Mast cells. Patrol ecm recognizing pathogens. Cause inflammation.

Question 21

Chemokines

Answer 21

Cell signals that recruit leukocytes to site of infection/damage. They work by increasing leukocytic affinity for integrin ligands during selectin mediated rolling. They also promote diapedesis.

Question 22

NK Cells

Answer 22

Perceive changes in infected cells (upregulation of activating molecules, downregulation of MHC-self complexes). Kill cells directly or produce cytokines to activate macrophages.

Question 23

Type 1 IFN

Answer 23

Produced by virus-infected cells, bind to uninfected cells which causes inhibition of viral protein synthesis, viral RNAase activity, and inhibition of viral protein expression.