Pod Parham 1

Front 1

What is vaccination?

Back 1

The priming of a human immune system for possible infection by inoculation with a deactivated form of the pathogen.

Front 2

The 2 primary lymphoid tissues

Back 2

Bone marrow and Thymus.

Front 3

What is a pathogen? What is an opportunistic pathogen?

Back 3

Any organism that can cause disease in humans. An opportunistic pathogen is usually a microorganism that lives comfortably in us until we get weakened, then it will become a problem.

Front 4

4 kinds of pathogens with at least one example. What kind does Kate like least?

Back 4

Bacteria: mycobacterium tuberculosis/salmonella enteritidis
Virii: Variola, HIV
Fungi: candida albicans, epidermophyton floccosum
Parasites: WORMS, protozoa: ascaris lumbricoides, trypanosoma brucei

Front 5

The external barrier between us and disease. The internal barrier?

Back 5

Skin. Mucosae.

Front 6

The two steps of initiating INNATE immune response.

Back 6

1. Recognition of the pathogen via any number of protein dependent methods - mostly cytokines.
2. Recruitment of effector mechanisms: complement+effector cells.

Front 7

General 4 step process of innate response.

Back 7

1. The complement is activated by unhappy tissues and covalently binds to the pathogen
2. The complement breaks into two pieces. One stays stuck to the pathogen (NEON SIGN: KILL ME) and one dissolves to call an effector (HEY COME HERE)
3. The effector cell receptor binds to the complement bound to the bacteria
4. Everybody gets eaten and phagocytosed.

Front 8

What is inflammation?

Back 8

Vasodilation by cytokines and the mass migration of WBCs into a site of infection. Cytokines also change the adhesion molecules in endothelium (remember selectins and integrins?) so WBCs know where to diapedese.

Front 9

The primary cell of the ADAPTIVE immune system?

Back 9

The lymphocyte.

Front 10

4 recognition mechanisms of INNATE immunity

Back 10

1. Rapid response
2. Fixed
3. Limited specificity
4. Constant effectiveness

Front 11

4 recognition mechanisms of ADAPTIVE immunity

Back 11

1. Slow as hell
2. Variable
3. Highly selective
4. Improves as responding.

Front 12

So what is adaptive immunity anyway? What does it ultimately enable?

Back 12

The selection and specification of our lymphocytes to a single pathogenic invader. Ultimately, this provides our bodies with a MEMORY of disease and quicker future response.

Front 13

Who attacks infection first and dies first? Who sticks around and cleans up?

Back 13

Neutrophils. Macrophages.

Front 14

Macrophages do 2 main things

Back 14

1. It will engulf entire bacterium.
2. It will recognize bacterial proteins and release cytokines.

Front 15

Dendritic cells

Back 15

Professional APCs. Enter a lymph organ with a dead cat in tow and tell everybody there's a cat-killer on the loose.

Front 16

Large granular lymphocytes vs small agranular lymphocytes

Back 16

NK cells that kill viruses vs. adapative immune cells that either are B cells or T cells.

Front 17

Cell surface receptor for B cells? For T cells?

Back 17

Immunoglobulins in the well known Y shape of heavynlight chains. . T-cell receptors that look like parallel lines with alpha and beta chains. Remember this by considering T cells are more specific, because they have less variable regions to adapt to an antigen.

Front 18

General flow of lymph. What happens in pathogenesis?

Back 18

From the tissues through afferent lymph vessels into a node out through an efferent vessel through the thorassic duct into the blood and repeat. If what's entering the node is pathogenic, the lymphocytes will stick around to start the adaptive response. Hence, swollen lymph nodes.

Front 19

Morphology of a lymph node

Back 19

The afferent lymph vessels enter the cortex and will encounter the lymphoid follicles first, where B cells are specialized. Further in the medulla are the T cell regions and then a single draining sinus. Not unlike a kidney. Within the lymphoid follicle are the germinal centers.

Front 20

What goes on in the lymph node when dendritic cells and bacterium arrive?

Back 20

Dendritic cells activate T cells, helper and killer. The killers bounce to go put the hurt on while the helper enter the germinal centers to DIFFERENTIATE B cells. Macrophages eat the bacteria. The differentiated B cells kick out antibodies. IMPORTANT: The entire lymphocyte population of a lymph node is from the blood. NO CELLS ARE BORN HERE.

Front 21

What happens if the lymph doesn't catch an infection and it enters the blood?

Back 21

Sepsis. Just kidding. The spleen will attempt to filter and kill blood borne illness.

Front 22

Components of GALT.

Back 22

Tonsils, adenoids, appendix, Peyer's Patches.

Front 23

What is an M cell?

Back 23

Special gut epi that detect pathogens and yank them out of the tract to the lymph.

Front 24

4 common elements of INNATE immunity.

Back 24

1. Noncov binding molecules that indicate a pathogen is present.
2. Cov binding molecules that give a binding site for phagocytes (NEON SIGN: KILL ME)
3. Phagocytes
4. Cytotoxic cells that kill virii.

Front 25

When a B-cell immunoglobin receptor molecules breaks off and enters the blood?

Back 25

It's an antibody.

Front 26

Epitope

Back 26

Part of the antigen bound by T and B.

Front 27

Isotype

Back 27

Special part of immunoglobin that tells it where to go or whatever. NOT on a T cell.

Front 28

Germline configuration

Back 28

The state of the DNA in T and B cells before any somatic recombination has occured.

Front 29

Somatic hypermutation

Back 29

When proliferating B cells do a switcheroo on nucleotides at TRANSLATION.

Front 30

What's a primary difference between T cell receptors and immunoglobins?

Back 30

Immunoglobins can bind to an intact pathogen, but T-cell receptors can only see the peptides of destroyed pathogens.

Front 31

What is the MHC?

Back 31

An individually specific array of cell-surface proteins that identify a cell as "self." The peptides that bind to the MHC are antigenic, and indicate the need for an immunoresponse. T-cells are ONLY able to bind to a peptide-MHC complex.

Front 32

Major difference between B and T cell binding.

Back 32

B cells recognize native proteins. T cells can ONLY SEE THE antigenic peptides bound to the MHC.

Front 33

What is an APC?

Back 33

A cell with a antigen-MHC complex that a T-cell can recognize.

Front 34

What are the two types of MHC molecules?

Back 34

1. MHC-I: present peptides from cells virally (intracellularly) infected. Cells with a peptide-MHCI complex are killed quickly by cytotoxic T cells.
2. MHC-II: present peptides from whatever pathogen the cell ingested from the ECM (extracellular digestion) to helper T cells. Only on phagocytosis-capable cells, like dendritic, macrophages, B cells. PAGE 24 and 25

Front 35

How do you tell the difference between a helper T cell and a killer T cell?

Back 35

Helper T Cell: CD4 glycoprotein
Killer T Cell: CD8 glycoprotein

Front 36

What cell does a TH1 talk to? What cell does a TH2 talk to?

Back 36

TH1: Macrophage.
TH2: B cell.

Front 37

2 steps of T cell clonal selection.

Back 37

1. Positive: picks T cells that can recognize the MHC well
2. Negative: eliminates T cells that bind to the MHC TOO well.

Front 38

Tolerance. Self-tolerance.

Back 38

The ability of T and B cells to not attack us. The ability of T and B cells to not attack each other.

Front 39

5 types of immunoglobulins

Back 39

IgA, IgD, IgE, IgG, IgM

Front 40

Humoral immunity

Back 40

Immunity conveyed by antibodies.

Front 41

2 main mechanisms for antibody combat

Back 41

Neutralization. Opsonization.

Front 42

Allergies

Back 42

Antibodies of IgE are made against common environmental stimuli. Which sucks.

Front 43

Autoimmune diseases.

Back 43

When the immune system decides to kill resident tissues.

Front 44

Whats the hygiene hypothesis?

Back 44

Reduce the occurence of inflammation, reduce the potential for a serious immunological response failure or event.