# T LYMPHOCYTE HYBRIDS & LYMPHOBLASTOID VARIANTS

> **NIH NIH R01** · UNIVERSITY OF WISCONSIN-MADISON · 1992 · $330,209

## Abstract

Three projects concerning regulation of the expression of class I
major histocompatibility genes in human lymphoblastoid cell lines
(LCL) will be undertaken. (1) Which DNA sequences regulate
transcription of the HLA-A, -B and -C genes?  The class I genes in
gamma ray-induced HLA antigen-loss mutants that have an
apparently normal gene but lack the corresponding mRNA will be
analyzed in order to answer this question.  (2)  The rate of
transcription of class I genes in B-LCLS is approximately 20 times
greater than that in T-LCLS.  Which DNA sequences and proteins
are responsible for this cell type-specific difference in
transcription?  Modified class I genes cloned in non-integrating
(pHeBo) vectors will be tested for expression by transferring them
into a class I-null B-LCL mutant and into class I-poor T-LCLs.
Nuclease protection an migration retardation in gels will also be
used to identify cell type-specific transcription regulatory
sequences.  Regulatory proteins will be sought on episomally
maintained class I genes.  (3) "5.4", "6.0" and "6.2" are cloned,
apparently normal, non-A, B, C class I genes for which
corresponding antigens are unknown.  They will be tested for
expression, before and after in vitro modification,, by transfer
into class I-null B-LCLs.  If antigens appear antibodies will be
raised against them and used to study their distribution in the
body.

Immunoprecipitation and electrophoresis will be used to study the
biochemical abnormality in B-LCL mutants that have a post-
transcriptional defect in class I antigen expression.

Transfer of cloned class II genes into class II-null mutant B-LCLS
will be used to create cells that have defined class II expression.
These cells will then be used to study aspects of antigen
presentation and T cell recognition.

Some human B-LCLS are deficient in surface expression of the
lymphocyte common antigen T200.  The T200 DNA, RNA and
protein of these mutants will be studied in order to determine the
cause of T200 deficiency.  Other T200 mutants will be isolated in
ways to be informative about the genetic regulation of T200
expression.

## Key facts

- **NIH application ID:** 3126196
- **Project number:** 5R01AI015486-14
- **Recipient organization:** UNIVERSITY OF WISCONSIN-MADISON
- **SAM.gov UEI:** LCLSJAGTNZQ7
- **Principal Investigator:** ROBERT Ivan DE MARS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $330,209
- **Award type:** 5
- **Project period:** 1978-12-01 → 1992-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3126196

## Citation

> US National Institutes of Health, RePORTER application 3126196, T LYMPHOCYTE HYBRIDS & LYMPHOBLASTOID VARIANTS (5R01AI015486-14). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3126196. Licensed CC0.

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