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HLA regulates postrenal transplant CML nonreactivity
Journal of Immunology (Baltimore, Md. : 1950)
|November 1, 1985
Summary
Kidney transplant patients with good graft function show donor-specific cell-mediated lympholysis nonreactivity (CML-NR). HLA-B and -C antigens, not HLA-A, are responsible for this in vitro nonresponsiveness, which can be overcome with IL-2.
Area of Science:
- Immunogenetics
- Transplantation Immunology
- Cellular Immunology
Background:
- Renal allograft recipients with functioning grafts exhibit donor-specific cell-mediated lympholysis nonreactivity (CML-NR) in vitro.
- The influence of the Human Leukocyte Antigen (HLA) system on CML-NR requires further investigation.
Purpose of the Study:
- To determine if the HLA system impacts the occurrence of CML-NR in renal transplant patients.
- To identify specific HLA antigens responsible for donor-specific CML-NR.
Main Methods:
- Immunogenetic studies involving in vitro stimulation of posttransplant lymphocytes from CML-NR patients.
- Use of unrelated healthy donor lymphocytes selected for the presence or absence of kidney donor-specific HLA antigens.
- Assessment of cytolytic nonresponsiveness upon stimulation with specific HLA antigens.
Main Results:
- Presentation of kidney donor-specific HLA-B and -C antigens induced cytolytic nonresponsiveness.
- Presentation of kidney donor-specific HLA-A locus antigens did not result in cytolytic nonresponsiveness.
- Nonresponsiveness was abrogated by the addition of exogenous interleukin-2 (IL-2), suggesting intact cytotoxic T lymphocytes.
Conclusions:
- Kidney donor HLA-B and -C antigens are critical for the in vitro donor-specific CML-NR observed in renal allograft recipients.
- HLA-B locus matching can suppress responses to HLA-A locus antigens.
- The observed nonresponsiveness is not due to a lack of specific cytotoxic T lymphocytes but rather an active regulatory mechanism possibly influenced by HLA-B/C expression.