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H Festenstein

Publications and source records attributed to H Festenstein.

At least 127 records · Page 7Linked to original sources
PubMed1981

MHC specified lymphocyte activating and suppressor activating determinants in human mixed lymphocyte reactions.

We have shown (1) the presence of HLA-linked Sad/s on a homozygous typing cell (HTC), FPA (8W321). When we used it to type the P family, which included an HLA-B/DR recombinant sibling, its genes mapped towards the HLA-B-A end of the HLA haplotype separate from HLA-D/DR and was found to be associated with HLA-Bw35 homozygosity; (2) this same recombinant maps the C4 complement genes on the HLA-D/DR end of the chromosome away from HLA-B; (3) that the suppressor T cell subpopulation which was activated by the Sad of this consanguineous HTC FPA was left behind after separating the OKT4 positive cells with a monomorphic monoclonal anti-T-cell antibody (OKT4). These OKT4 positive cells reacted normally in MLC to the FPA Lad Fes 6; (4) that at least part of the genetic control of suppressor recognition is outside the HLA complex.

Chromosome Mapping↗
PubMed1981

Intra HLA-D region recombinant maps HLA-DR between HLA-B and HLA-D.

A consanguineous family has been typed for HLA-A, B, C, D, DR and GLO, Bf, C2 and C4 and other red cell markers. The results indicate that an expected Dw7 homozygous sibling is a "Dw1"/Dw7 recombinant, probably derived from a crossing over between DR and D on the paternal haplotypes. The anomalous typings by Dw1 HTCs of the recombinant haplotype are best explained by the likely presence of an additional Lad polymorphism which could be a serologically detectable second epitope on the same molecule as the HLA-D determinant or in the form of two linked chains, one encoded by HLA-D and one by another Lad gene in the HLA haplotype.

Blood Grouping and Crossmatching↗
PubMed1981

HLA A and B locus antigens in patients with unexplained hepatitis following halothane anaesthesia.

HLA A and B locus antigens were determined in 17 patients who had recovered from unexplained hepatitis following halothane anaesthesia. The greatest deviations from expected frequencies were observed with A1, A11 and BW22, but these differences were not statistically significant when the P values were corrected for the number of antigens tested. Although a larger series might show such deviations to be significantly different, HLA typing is of no predictive value in determining those at risk to hepatitis following repeated halothane exposure.

Adult↗
PubMed1981

Sources of variance in the double normalized value: an evaluation of its reproducibility as a measure on HLA-D locus identity.

Two different sets of mixed lymphocyte culture (MLC) experiments were performed using HLA-D homozygous typing cells (HTC). In all stimulator-responder combinations the median cpm's of four replicate cultures were reduced into double normalized values (DNV). In the first experimental set the responder panel was unselected, whereas the responders for the second set were chosen on the basis of either sharing an HLA-D determinant with the stimulator (ID) or not (non-ID). The experiments were designed: Set 1: To estimate the technical variability in the DNV's and to observe the distribution of this variability. The standard deviation of an observation on a stimulator-responder combination was approximately 24 DNV units. Thus, by running 6 experiments on each responder we would have a mean DNV with a standard error of 10 DNV units. Set 2: To determine whether stimulators typing for the same Dw specificity had the same distribution of DNV's and to investigate the variability between responders, between experiments and within experiments. Although the mean DNV is the same for all HTC's, the variability in observations was greater for some HTC's than for others. The variability may be completely technical for some HTC's, whereas for other HTC's there is evidence of responder variability and between experiment variability. Important implications of these results are: (1) that in using a single cut-off value of 60 for all HTC to define typing responses one will have a very high misclassification rate for a large percentage of ID responders; (2) for some HTC this error rate can be reduced through repeating the experiment 4 times and raising the cut-off point; (3) this error, together with the technical and/or experimental variance can be further reduced by using 2 or more HTC's of the same specificity in each experiment and by combing their data; (4) misclassification can be reduced in every situation by doing 4 experiments, using 2 HTC per responder and computing a cut-off which gives a misclassification rate for each Dw type of 10% in ID's and in non-ID's. Thus the best approach to achieving Dw locus typing with a desirable low rate of misclassification would be to do similar control studies of every HTC, to estimate technical experimental and responder variance and then use this information to determine a cut-of value and the number of HTC's and experiments per responder required to keep the error rate at a satisfactory level.

Cells, Cultured↗
PubMed1981

Incompatibility for or pre-immunization against M1s determinants decreases lethal graft-versus-host reaction developed across non-H-2 and/or H-2 barriers.

The effect of incompatibility for M1s determinants was studied in lethal graft-versus-host reaction (GVHR) in the mouse. GVHR was induced in adult recipients of the following H-2k strains: (AKR x B10.BR)F1 (Mlsa/Mlsb); (C3H x B10.BR)F1 (Mlsc/Mlsb); (CBA/J x B10.BR)F1 (Mlsd/Mlsb) and (CBA/H x B10. BR)F1 (Mlsb). Recipient mice were heavily irradiated and grafted with bone marrow and spleen cells from H-2 compatible B10.BR (H-2k, Mlsb) or H-2 incompatible B10.D2 (H-2d, Mlsb) or B10 (H-2b, Mlsb) strains. The cells from B10.D2 and B10 donors were normal, while those from B10.BR donors were either normal or pre-immunized against the recipient strains. In all experiments the survival of recipients with Mlsa/Mlsb and Mlsd/Mlsb phenotypes, and only in one experiment of those with Mlsc/Mlsb phenotype was greater and/or the survival time longer than that of recipients expressing only Mlsb. However, late deaths (greater than 120 days post grafting) observed after grafting of normal B10.BR cells were more frequent in Mlsd/Mlsb than in Mlsb strains. On the other hand, when B10.BR donor cells were pre-immunized against H-2k compatible (AKR x B10.BR)F1 (Mlsa/Mlsb) or (CBA/J x B10.BR)F1 (Mlsd/Mlsb) strains, the survival time of H-2 incompatible (B10 x B10.BR)F1 (H-2b/k, Mlsb) recipients was longer than when donor cells were pre-immunized against (CBA/H x B10-BR)F1 (Mlsb) strain. We conclude that donor incompatibility for Mlsa or Mlsd or donor-pre-immunization against Mlsa or Mlsd exerts a protective effect on lethal GVHR developed across non-H-2 or H-2 barriers; the protective effect of Mlsc is less efficient or absent. The Mls-induced protective effect shows the following properties: (a) efficiency in vivo correlates with the capacity of the corresponding alleles to stimulate an in vitro MLR; (b) is efficient in either primary or secondary response to other minor antigens; (c) is not H-2 restricted; (d) is nonspecific; (e) disappears late after grafting; (f) with respect to the genetic background, the early protective effect is followed, late after grafting, by an opposite effect which increases the mortality, suggesting that Mls locus determinants are capable of activating several cell populations with different biological functions.

Animals↗
PubMed1980

Precursor and effector phenotypes of activated human T lymphocytes.

In mice, thymus-derived lymphocytes are differentiated into functional subclasses by their cell surface antigens. The Ly 1 determinants are present on T cells with a helper function, whereas Ly 2 and Ly 3 antigens are expressed on the surface of lymphocytes with suppressor or cytotoxic functions. In man also, T-cell subsets have been identified using allo- and heteroimmune sera and, more recently, using monoclonal antibodies, which seem to identify helper and suppressor or cytotoxic subpopulations. The major histocompatibility system (MHS)-encoded Ia antigens belong to several polymorphic families of membrane associated glycoproteins originally found on B lymphocytes; however, they have also been shown to be markers for suppressor T cells in mice. Recent studies have shown that in both mouse and man, T cells activated by a mixed lymphocyte reaction or by mitogens become Ia+. Furthermore, some human T lymphoid cells, either freshly isolated from peripheral blood or after in vitro activation by lectins or alloantigens, possess suppressor properties. We report here the phenotype of a T suppressor-cell subpopulation which was induced in long-term culture of lymphoid cells after activation with phytohaemagglutinin (PHA). Our results suggest that a subset of T cells was progressively expanded over a period of 8 days in culture and that, with the expression on the surface of these cells of 'Ia-like' antigens, they acquired the capacity to suppress the proliferative response of syngeneic or allogeneic lymphocytes to alloantigens or mitogens.

Antigens, Surface↗
PubMed1980

Human alloimmune sera against T cell subsets. Detection and influence on pokeweed mitogen-stimulated Ig production in vitro.

Sera from multiparous women contain antibodies against T cell subsets. Population and family studies of four anti-T cell-subset antibodies are given. Two of these reacted with part of the suppressor T cell fraction (T gamma) and two with part of the helper T cell fraction (T mu) cells. By mixing T gamma- and mu-enriched cell suspensions in different concentrations, preliminary evidence was obtained that the anti-T cell-subset sera recognized T cells that had different functions in pokeweed mitogen-stimulated cytoplasmic immunoglobulin synthesis.

Adult↗
PubMed1980

Type 1 diabetes and the HLA-D locus.

HLA-D specificities have been investigated in 58 classical Type 1 diabetics and 43 healthy subjects. Both groups were selected according to the HLA-B locus antigens which are known to have a significant positive or negative association with the disease. The results indicate that (1) the primary association of the disease is with HLA-DW3, (2) the increased frequency of DW4 in diabetics with rare exception is co-existent with the presence of DW3, (3) the low frequency of DW2 is secondary to the increase in DW3 and/or DW4, and is not consistent with a primary 'protective' role. It is suggested that these data support the hypothesis of interaction between HLA-linked genes operating by separate mechanisms to confer the susceptibility to young onset Type 1 diabetes (Type 1 A).

Adolescent↗
PubMed1980

HLA-A, B and C antigens in South Indian families with leprosy.

Seventy-two families, selected for having at least two children affected with leprosy, were HLA typed for 57 A, B and C locus antigens recognized by the WHO Nomenclature Committee. In addition, 20 possible new "splits" were investigated. The distribution of A, B and C locus antigens in affected and unaffected family members was similar, irrespective of the type of leprosy in the family. Gene frequencies (derived by direct gene counting from 253 haplotypes), haplotype frequencies and delta values were calculated. There is evidence for heterogeneity of B5, B15, B17, Bw16 and Bw35 and for the existence of at least one A locus and one B locus antigen not previously detected. The value of the HLA system for detecting expaternal children in a highly inbred population and the effect of inbreeding on the HLA system is discussed.

Chromosome Mapping↗
PubMed1980

Serological and immunochemical studies of H-2 allospecificities on K36, a syngeneic tumour of AKR.

Expression of H-2 antigenic specificities on K36, a spontaneous leukaemia originating from AKR (H-2k) mice, was studied by serology and immunochemistry. Two ascites lines of the tumour, as well as a tissue culture adjusted and cloned tumour line, were used in these studies with similar results being obtained. K36 expresses on its cell surface D-region encoded H-2K antigens but does not express K-region encoded H-2K alloantigens. It also expresses on its cell membrane, H-2 specificities of foreign haplotypes not present on normal AKR lymphoid cells. The molecular basis of the H-2Dd specificity on K36 (H-2k) was analysed by immunoprecipitation and polyacrylamide gel electrophoresis. The specificity was shown to be present on a glycoprotein of apparent molecular weight 45,000. However, antisera against the H-2Dd private specificity (H-2.4) precipitate additional glycoprotein of 45,000D and also 70,000D. In tryptic peptide maps of the isolated 45,000D fraction precipitated by anti-H-2.4 serum from radiolabelled K36 glycoprotein, all H-2Dd specific peptides were present in the same quantitative ratio. This is consistent with the structural identity of the foreign H-2Dd from the K36 tumour with normal H-2Dd and supports the hypothesis of a regulator system controlling the H-2 allelism. Under certain circumstances such a system could cause suppression of one and derepression of the other H-2 gene products.

AKR murine leukemia virus↗