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C Mawas

Publications and source records attributed to C Mawas.

At least 91 records · Page 5Linked to original sources
PubMed1981

Cross-reactions between mouse Ia and human HLA-D/DR antigens analyzed with monoclonal alloantibodies.

Two mouse monoclonal anti-I-E/Ck alloantibodies (H7-8.26 and H10-81.10) directed against 2 distinct determinants of the specificity Ia-7 and 1 anti-I-Ak alloantibody (H8-15.9) directed against a public determinant common to the I-A subregion products of the H-2k, H-2b, H-2d, H-2q, and H-2ja haplotypes identified cross-reactive determinants on lymphoid cells from various mammalian species, including rat, dog, pig, cow, hamster, and guinea pig. In man, these antibodies detected nonpolymorphic determinants of DR antigens on B cell-enriched peripheral blood lymphocytes from 50 unrelated individuals. These cross-reactive DR determinants were also detected on lymphoblastoid B cell lines, on PHA-activated peripheral T lymphocytes, and on allospecific cytolytic T cell clones, but not on various DR-negative human T leukemia cell lines. Two chains of 29,000 and 35,000 daltons m.w., corresponding to DR antigens, were precipitated by H7-8.26 and H8-15.9 antibodies from radiolabeled membrane extracts of Raji cells. Competitive binding experiments indicated that the 3 mouse anti-Iak antibodies identified 3 distinct cross-reactive determinants on human cells. The results indicate that: a) The cross-reactivity described between mouse I-E/C gene products (Ia-7) and human DR antigen(s) involves, in fact, several distinct and topologically distant determinants. b) At least 1 determinant cross-reacting with DR can be identified on I-Ak gene products. c) The intriguing genetic problem of mouse MHC allotypic determinant(s) being nonpolymorphic in man cannot be simply explained by the deletion of an I-E alpha chain in some strains of mice.

Absorption↗
PubMed1980

Production, expansion, and clonal analysis of T cells with specific HLA-restricted male lysis.

A cytotoxic T cell (CT) lines grown as a population (CT line) was initiated from the peripheral blood lympocytes (PBL) of a female aplastic anemia patient who was known to express CT that were able to lyse HLA-A2-positive male cells. The anti-H-Y HLA-A2-restricted cytotoxic activity could be maintained over prolonged periods of time. The CT lines could be expanded and maintained in culture for >65 d by the use of mitogens and irradiated feeder cells. Out of 68 cultures obtained after cloning of the CT lines, 43 showed varying, but always specific, anti-H-Y HLA-A2-restricted lytic capacity on a per-cell basis. We could show that the cloned cultures were composed of >80% T cells that carry the HLA-A, -B, -C, and also the HLA-DR antigens identical to the original PBL.

Anemia, Aplastic↗
PubMed1980

Split of HLA-D into two regions alpha and beta by a recombination between HLA-D and GLO. I. Study in a family and primed lymphocyte typing for determinants coded by the beta region.

In a family with a paternal recombinant child between HLA-D/Dr and GLO, PLT have been raised between HLA-A-B-C-D-DR and Bf identical sibs. Since these sibs differ only within a region (beta) between HLA-D/DR and GLO and the centromere, these PLTs allow the typing of two new determinants differing from HLA-D/DR, possibly alleles at a new locus mapping in a region outside HLA-D/DR. A difference limited to this beta region can induce a weak primary and a strong secondary MLR.

Chromosome Mapping↗
PubMed1980

Expansion of human lymphocyte populations expressing specific immune reactivities. II. A comparison of immune reactivities in human T lymphocyte lines derived from allogeneically primed cultures and maintained with lectins or conditioned medium.

In a previous paper, lectins were shown to allow a strong expansion of in vitro primed cells; among the lectins tested, PKW but not PHA (nor Con A) was found to reactivate CTLs. We then asked two further questions: Could one maintain a long term expansion of human T cells using iterative lectin stimulation? And, if so, could the immune reactivities, once expressed in the original primed cells, also be maintained? We report here that lectins remain potent mitogens for primed cells, and allow good expansion over many cycles, provided fresh irradiated cells (autologous or not to the responder) are added to the cultures. When PKW is used as the iterative mitogen, both the specific proliferation (PLT) and the specific cytotoxicity are maintained after each cycle. When PHA is the iterative stimulant, only the specific proliferation (PLT) is maintained, while no measurable cytolysis is present. However, if iteratively PHA stimulated primed cells are now cultured in the absence of PHA, even without additional specific stimulation, cytolytic activity is recovered from the cultures. In parallel, primed cells iteratively expanded using conditioned medium appear to retain both their specific lytic function and their specific proliferative function. Preliminary data suggest that the cloning efficiency when using lectins is higher than when using conditioned medium.

Cells, Cultured↗
PubMed1979

The in vitro cellular response of human lymphocytes to trinitrophenylated autologous cells: HLA-D restriction of proliferation but apparent absence of HLA restriction of cytolysis.

Primary as well as secondary proliferative and cytotoxic responses to 2,4,6-trinitrophenyl (TNP)-modified autologous human cells have been studied. Proliferative responses have been obtained both by primary (peak on day 6) and secondary (peak on day 2--3) stimulation. Both responders and nonresponders were found among the panel of unrelated individuals tested. All responders in a secondary reaction also gave significant primary responses. Intrafamilial studies showed that the ability to restimulate a proliferative response followed the major histocompatibility complex haplotype of the responder; in some cases, the two haplotypes differed in their ability to restimulate. Using unrelated individuals typed for HLA-A, B and C, as well as HLA-D and DR, proliferation was shown to occur only when the unrelated stimulator shared HLA-D region products with the responder. In contrast, no HLA restriction was found in cell-mediated lympholysis (CML) (neither in primary nor in secondary responses) in most cases. The data suggest that the observed killing is independent of sensitization. Both responders and nonresponders in proliferation yielded high levels of lysis; no increase of lysis was found in kinetic studies; most allogeneic CML combinations were highly lytic for the TNP-modified responder cells at a time when the lysis of the specific allogeneic target is negligible. These preliminary data suggest that the killing observed might be different from classical T cell-mediated lympholysis.

Cytotoxicity, Immunologic↗
PubMed1979

Specific inhibition of human lymphocyte responses by primed autologous lymphocytes. I. Evaluation of MLR inhibition as a model for suppression.

Human lymphocytes from person A, primed for 10 to 14 days in MLC against lymphocytes from person B, inhibit specifically the proliferative response to B by fresh (i.e., unprimed) lymphocytes of A. Gamma-irradiated (2000 R) primed lymphocytes likewise inhibit specifically, although less strongly. Cells of A, primed with cells of B and then irradiated, usually can inhibit the response of A to cells of any individual sharing HLA-D antigens with B, and the effect tends to be independent of the number of stimulating cells. We also often see inhibition of responses to cells sharing HLA-A and -B antigens with person B, but this effect tends to be lost when the number of stimulating cells is increased. Similarly, at low doses, cells primed for HLA-D antigen a appear not to inhibit the response to an irrelevant HLA-D antigen b on the same stimulating cell. At higher doses of primed cells, even the response to the irrelevant antigen is inhibited. These data suggest to us that at least two mechnaisms may be involved: one directed at the stimulating cell (most likely cell-mediated cytolysis), and predominant at high ratios of primed cells to stimulating cells; the other directed at specific clones of responding cells, and predominant at low ratios.

Dose-Response Relationship, Immunologic↗
PubMed1978

A weak human MLR locus mapping at the right of a crossing-over between HLA-D, Bf and GLO.

An unexpected MLR reaction has been observed between three HLA-identical sibs; it consists of bidirectional positive MLR between identical female twins and a sister. No argument for a lymphoid mosaic could be found, although twins were frequent in the family; similarly no HLA-A/B or HLA-B/D recombinant could be demonstrated. The MLR, although weak, was highly reproducible. PLTs could be raised between the sibs, without an apparent segregation in this family nor in five other families, but such PLTs discriminated well between the positive and negative controls. In the absence of any proof that such a weak MLR locus could be on another chromosome than chromosome 6, two lines of argument are indirect evidences that such a locus could be indeed on chromosome 6: one of the sibs differs from the two others for two markers outside HLA--D--DR--Bf: glyoxalate (GLO) and red blood group P.

Blood Group Antigens↗
PubMed1977

Suppression of generation of human cytotoxic effectors by lectins or lectin-activated peripheral blood lymphocytes.

The lectins phytohemagglutinin, pokeweed mitogen and concanavalin A used at their optimal mitogenic concentration, or human lymphocytes activated by the same mitogens, were found to suppress the in vitro generation of cytotoxic effectors when added to a cell-mediated lympholysis (CML) mixture during the first 48 h of culture. The data suggest that the suppressive mechanism is mediated to a greater extent by an allogeneic interaction between lectin-activated cells and the allogeneic cells present in the CML mixture than by suppressor cells induced by the lectin. Since partial suppression was observed with supernatants of activated lymphocytes cultured for 18 h with allogeneic stimulating cells (but not activated lymphocytes alone), a soluble mediator may be involved in the suppressive mechanism. The mechanism of suppression therefore may be identical to the preemption phenomenon recently described in primary and secondary CML.

Antigens↗
PubMed1977

Detection of HLA-D clusters using primed LD typing.

Using a set of 17 primed LD typing (PLT) cells tested on a panel of 35 unrelated cells, we showed that certain groups of PLT cells tended to detect similar unrelated cells. The PLT cells were grouped into seven clusters and these tended to correlate with the seven HLA-D specificities represented on the panel, as determined by HTC testing. These data suggest that the antigens that cause restimulation in PLT are similar to those HLA-D antigens detected by the homozygous typing cell (HTC) test or, alternatively but more unlikely, that the two typing methods are detecting genes in close linkage disequilibrium with the HLA-D region.

Epitopes↗
PubMed1977

Detection by three cellular immunological techniques of the antigenic determinants of the Ly-Li system, expressed on human B lymphocytes.

A clear correlation was observed between the presence of an Ia-like antigenic B-cell system Ly-Li, detected serologically, and three cellular immunological techniques: [1] mixed lymphocyte reaction (MLR) inhibition by an anti-Li antiserum; [2] level of restimulation of anti-Ly-Li in-vitro-primed lymphocytes; and [3] detection of HLA-D alleles by homozygous typing cells. These results suggested that the allelic products detected serologically may be identical to those detected by the first two techniques, namely MLR inhibition and in-vitro-primed lymphocyte typing, and, possibly, HLA-D typing using homozygous typing cells, although the correlation was repeatedly found to be less clear for the last technique.

B-Lymphocytes↗
PubMed1977

Detection of HLA-D clusters and segregation studies using primed LD typing.

By testing a group of PLT cells over a panel of unrelated restimulating cells, the PLT's could be grouped into clusters according to their ability to discriminate antigen(s) in unrelated cells. The PLT clusters broadly correlated with the homozygous typing cell-defined HLA-D clusters represented on the panel. The PLTs grouped together clearly segregate with a particular HLA haplotype when tested in both unrelated families not possessing the sensitizing haplotype and in the family with the sensitizing haplotype. No influence of HLA SD antigens could be observed in PLT restimulation in the segregation studies.

Epitopes↗