Cornell University BIOG 1105-1106
Unit 5: Demos

Objective 1:

How inflammation works (interactive animation from Time magazine)
Immunology animation (optional)

Objective 9:

Complement system (9c) (much of this is supplemental)
Be the phagocyte!  Play the Immune System Defender Game
Immune response video (right click to download here or watch DVD in study center)
Immune response handout to accompany video

Objective 10:

The role of interleukins in the defensive response (10c)

Objective 11:

Booster shots and the role of memory cells (11b)
See optional links below for more information on vaccines and immunology
Poultry eggs may yield snake antivenin (optional)

Objective 12:

Autoimmune diseases result from a failure of "self-tolerance" (optional)
Multiple Sclerosis (optional)
Rethinking MS: multiple sclerosis may not be an autoimmune disease after all.
Lupus (optional)
Type-1 Diabetes (optional)
Publicly accessible MHC database for transplant / donor matching (optional)

Objective 13:

HIV and helper T cells
See optional links below for more information on HIV / AIDS

Objective 14:

What permits metastasis? (14b)
Scientific American: How Cancer Arises (available in Study Center; PDF available on Blackboard)

Objective 15:

Telomeres (15d)
Fix Those Genes or Else: defects in DNA proofreading can prompt tumors (optional)

Objective 16:

Scientific American: How Cancer Spreads (available in Study Center; PDF available on Blackboard)

Objective 17:

Risk factors for cancer
Immunotherapy for cancer (optional)
Learn more (from the American Cancer Society)
See optional links below for more information on cancer

Objective 18:

American Scientist: DNA Vaccines as Cancer Treatment (available in Study Center; PDF available on Blackboard)
HPV Vaccine: Info from the CDC
Cancer Vaccines (optional)
Scientific American: (available in Study Center; PDF available on Blackboard) (optional)

The role of interleukins in the modulatory action of T lymphocytes

Helper cells become aware of the presence of an antigen when it is exposed in the binding cleft of an MHC-II protein.  Whether the antigen is displayed by a B cell or a presentation cell, only a helper cell specific for the antigenic determinant and the MHC-II molecule holding it can bind and become activated.  An activated helper can advance the campaign against the antigen and its source in several ways.  First it installs receptors for a chemical signal molecule, interleukin, in its own membrane; then it begins secreting interleukin.  The binding of interleukin to its own receptors causes the helper cell to proliferate (see figure).  The secreted interleukin also induces multiplication of any activated cytotoxic T cells nearby that have recently encountered their specific antigens; more often than not, the helper cell and its cytotoxic neighbor will be responding to the same pathogen.

When bound to stimulated B lymphocytes, helper T cells produce an interleukin that encourages the B cells to secrete antibodies.  Yet another kind of interleukin energizes nearby macrophages.

Modulatory action of T lymphocytes.  (A) Helper cells regulate the humoral immune response by binding to B lymohocytes that display a unique antigen.  (B) The bound helper  secretes various interleukins, one of which causes the helper to multiply; another form of interleukin induces the B cell to secrete antibodies, which bind he antigens on the invading cell (A). (C)  In the cell-mediated responsce (which normally would be active simultaneously only if the invading microorganisms can infect host cells), a third kind of interleukin induces nearby bound cytotoxic T lymphocytes to kill their targets.  (D) A fourth interleukin activates nearby macrophages to ingest antibody-marked targets.

From Gould and Keeton, Biological Sciences, 6th edition

   
© 2010 | BIOG 1105-1106