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Related post: an endocytic compartment where it dissociates from class II prior to the binding
of immunogenic peptides and the cell surface appearance of peptide/class II
complexes. It had been suggested that superantigens utilized the invariant chain
binding site of class II molecules. However, our data have shown that the binding
site of HLA-DR for the seven toxins tested was distinct from that for the HLA-DR-
associated invariant chain. In addition, cell surface class Il/invariant chain
complexes were still able to stimulate T cells by superantigen. An important
implication from this finding is that endogenous superantigens encoded by
pathogens may bind to class II molecules intracellularly prior to the dissociation
of the invariant chain (Malnati, Roche, Pinet, Gueguen).
NK Cell Specificity
Natural Killer (NK) cells are thought to play a role in the control of viral infection
before the establishment of a specific cytol5^ic T cell response mediated by CD3-
positive MHC-restricted T cells. Recently, specific recognition of alloantigens by
NK cells was reported. Most of the cells displaying NK activity belong to the CD3-
CD4-CD8-CD16+CD56+ subset of peripheral blood lymphocytes. The aim of this
study is to determine the degree of target cell specificity displayed by NK clones,
and to eventually define the mechanism of target cell recognition by NK cells. As
a first step, it was established that NK clones from a normal individual were able
to specifically recognize and kill normal cells from the same individual that had
been infected in vitro with Human Herpes Virus 6 (HHV6). However, only about
half of the clones (58/118) were able to kill human Herpes virus 6 (HHV6)-infected
autologous PHA-blasts, while all of them lysed the NK-sensitive cell line K562. A
group of clones from two individuals were further characterized for their ability to
recognize autologous and allogeneic infected cells. The results showed for the
first Suminat 50 time that specificity in target cell recognition by NK cells is controlled at
several levels: first, at the level of the NK clone itself, and second, by genetically
variable elements on the target cells. Because the cell surface level of class I
MHC molecules was virtually unaffected by HHV6 infection, recognition by NK
cells of these particular targets cannot be explained by the mere absence of class I
molecules, as was proposed to explain the Suminat Nasal Spray NK-mediated killing observed in other
systems. Future studies are directed toward definition of the molecules involved
in this critical first line of immune defense (Malnati, Wagtmann).
Cytokines Modulate the Antibody Response to SSS-IQ Buy Suminat in vivo.
Previous studies demonstrated that suppressor T cells (Ts) can be influenced by
cytokines. The present studies were designed to examine the effects of cytokines
on amplifier T cell (Ta) activity by the administration of various C5rtokines at peak
amplifier activity i.e. two days post-immunization with SSS-III. Treatment of
mice with recombinant IL-6 or IL-5 increased the magnitude of the antibody
response to SSS-III. Further, treatment with TGF b increased the secretion of
IgA when this cytokine is given 2 days post-immunization. These findings
suggest that the activity of both Ts and Ta cells is influenced by c3rtokines. (Taylor,
Modulation of Antibody Response to Pseudomonas LPS by IL-4.
Previous studies showed that the predominant IgG isotype produced in response
to Pseudomonas aeruginosa LPS (PALPS) is IgGs. We showed recently that when
recombinant IL-4 is given all IgG isot5T)es (and IgM) are enhanced. Likewise,
when anti-IL-4 antibody (llBll) is given the PALPS-specific antibody response
was decreased for each isotype. However, treatment with llBll antibody
increased total IgM S3nithesis, without affecting total IgG. While it is clear that
IL-4 can influence the antibody response to PALPS the underlying mechanisms
remain to be resolved. (Taylor, Baker).
LABORATORY OF IMMUNOGENETICS
October 1, 1991 to September 30, 1992
HONORS AND AWARDS
Dr. Thomas Kindt, Chief of the Laboratory of Immunogenetics, was an invited
participant in a meeting on pathology and HIV infection in Hamburg, Germany.
He was also invited to chair a workshop on animal models for AIDS at the
International Congress of Immunology in Budapest, presented one of the keynote
addresses at a meeting on biosafety and HIV/retrovirus research in Durham,
North Carolina and presented laboratory data at the meeting of the Laboratory of
Tumor Cell Biology in Washington, D. C. In addition, laboratory data were
presented at the University of Connecticut, at the CDC in Atlanta, at Wright State
University in Dayton, Ohio, at the meeting of the Experimental Immunology
Branch of the NCI, at Hybridtech Incorporated and at the Bristol-Meyer Scribb
Institute in Seattle. Members of Dr. Kindt's research section also presented data
at the meeting of the FASEB in Anaheim in California. In July of 1992, Dr. Kindt
finished a five year term as Deputy Editor of the Journal of Immunology and a 15
year term as Associate Editor of the Journal of Experimental Medicine. At the
same time he was appointed Associate Editor of the FASEB Journal and remains
North American regional editor of Research in Immunology. Dr. Kindt serves on
the Board of Scientific Visitors for the Oklahoma Medical Research Foundation in
Oklahoma City and serves in a similar capacity for the Research Program at the
Virginia Mason Institute in Seattle, Washington. The Multiple Sclerosis Society
awarded Dr. Kindt their Hope Award for completion of a six-year term as
reviewer for research projects for the Multiple Sclerosis Society. Dr. Kindt
continues to serve on the NIH Allergy and Immunology Study Section and serves
on the scientific advisory boards of Oncor Inc., Gaithersburg MD, Innovir
Laboratories Inc., New York, NY and served an ad hoc term on the SAB of TSI
Inc, Worcester, MA.
Dr. Phillip Baker presented lectures and seminars at several universities and
medical schools. He is on the Editorial Board of the ASM News , serves on the
Public Relations Committee of the American Society for Microbiology (ASM) and
also serves on the Publications Board of the International Endotoxin Society (lES).
He was invited to give the Board of Education and Training Lecture, "Update '92
in Regulatory T Lymphocytes", at the annual meeting of the ASM in New
Dr. Christopher Taylor was invited to convene a symposium on "Mechanisms of
protective immunity: cytokines and isotype-specific antibody responses" at the
annual meeting of the American Society for Microbiology, in New Orleans, LA.
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