> Here we go! As previously noted, I am working on a companion volume
> for a new edition of a major cellbiology text, and am in charge of
> generating questions about such diverse topics as immunology,
> cytoskeletons, ECM etc. The first chapter is immunology; this will be
> crossposted to cellbiology and immunology. Any and all responses will
> be greatly appreciated; all respondents will get credit in the preface
> of the companion volume. Have a go at these, and thanks in advance
>> Dave
> ---
> Dave Rintoul Internet: drintoul at ksu.ksu.edu> Biology Division - KSU Latitude 39.18, Longitude -96.34
> Manhattan KS 66506-4901 Compuserve: 71634,32
> (913)-532-6663 or 5832 FAX: (913)-532-6653
>> ideas for higher level questions - I am not an immunologist and I have
> only some vague ideas about the answers to some of these questions.
> Any help would be appreciated, as would ideas for other questions in
> the same vein.
>> 1. In the textbook it states that patients with SCID (severe combined
> immunodeficiency) "previously could be kept alive only in s sterile
> environment, but now can be cured by bone marrow transplantation.
> Patients lacking a suitable marrow donor re being treated
> experimentally by gene therapy." My response to this is: What
> constitutes a suitable vs unsuitable bone marrow donor for a person
> who completely lacks an immune response?
*********************
The problem in this case is not the immune response generated by the
host, but the response generated by the donor cells upon reconstitution
of the host with bone marrow. A sufficient genetic disparity between
donor and host will cause the initiation of "graft versus host
disease" (commonly known as GVH. This process is essentially an immune
response by the reconstituted immune system against the recipient
antigen bearing cells. This condition occurs in a high proportion of
bone marrow transplant recipients and can result in death if unchecked.
>> 3. Why do we have an MHC?
I beleive that the polymorphism of the MHC locus is an essential
survival characteristic that prevents the complete destruction of a
given species by a single pathogenic agent. The MHC molecule 1)
provides a means by which cells of the correct specificity can be
induced to meet (e.g. T cells and B-cells in cognate interactions) and
interact. 2) To direct effector responses towards the correct targets
(a classic example of this is virus infected cells. Cytotoxic T cells
are directed towards the destruction of cells that are the site of
virus production rather than being triggered by free virus in the
surrounding medium). 3) Polymorphism in MHC antigens similarly
produces a wide array of antigenic specificities that will be "seen" by
the immune system of different individuals, thus if an organism manages
to avoid immunologic recognition because it looks like "self" it is
unlikely to appear that way to everyone because of the polymorphism of
the MHC.
I don't know if I am completely clear. Please ask if you need to.
==============================================================================
James F. George, Ph.D. "Back off man, I'm a scientist"
Department of Surgery --Bill Murray
University of Alabama at Birmingham
205-934-4261 voice
txpljfg at uabcvsr.cvsr.uab.edu
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