Biomedical subjects

F Bekkhoucha

Publications and source records attributed to F Bekkhoucha.

6 recordsLinked to original sources

PubMed1993

[Congenital C1-esterase inhibitor deficiency. A study of 4 Algerian families].

We present the results of a preliminary study (the first of this kind in Algeria) in which 4 families presenting with congenital deficiency of the C1-esterase inhibitor (C1-INH) responsible for hereditary angioneurotic oedema were biologically explored. The complement fractions C1-INH, C4 and C3d were assayed in 38 subjects of the 4 families. Extending this biological evaluation to all members of theses families enabled us to identify all asymptomatic subjects (46 percent in our series). In 2 patients the congenital disease was associated with systemic lupus erythematosus. Some clinico-biological discordances are reported and discussed in the light of data from the literature.

Adolescent↗

PubMed1985

L3T4 but not LFA-1 participates in antigen presentation by Ak-positive L-cell transformants.

We report that mouse L cells expressing Ak class II molecules on their surface after DNA-mediated gene transfer are capable of presenting the synthetic copolymer (Glu60 Ala30 Tyr10) to Ak-restricted long-term T-cell clones. Antigen-induced T-cell stimulation could be inhibited by monoclonal antibodies (mAb) directed at spatially distinct determinants of the alpha and/or beta subunits of the Ak molecule, and by the rat L3T4-specific mAb H129.19. In contrast, several rat mAb reactive with the mouse LFA-1 molecule failed to inhibit T-cell activation when L cells were used as antigen-presenting cells (APC), although these mAb strongly inhibited the same T-cell responses in the presence of leukocytic APC. Similarly, the cytolytic activity of the Ak-specific T-cell clone A15.1.17 was blocked by L3T4-specific and by LFA-1-specific mAb when tested on Ak-positive B-cell hybridomas, but only by L3T4-specific mAb and not by LFA-1-specific mAb when Ak-positive L-cell transformants were used as targets. These data support the notion that the LFA-1 molecule is not necessary for T-cell activation, and suggest that its functional role as an accessory molecule depends on the leukocytic nature of the APC tested.

Animals↗

PubMed1984

Efficiency of antigen presentation to T cell clones by (B cell X B cell lymphoma) hybridomas correlates quantitatively with cell surface ia antigen expression.

A series of B cell hybridomas was used as a model system to assess quantitatively the role of Ia molecules in antigen presentation to allo- or soluble antigen-reactive T cell clones. These hybrid cell lines were established by fusion between the HGPRT-BALB/c B cell lymphoma M12.4.1 and LPS-stimulated spleen blasts from B10.BR (H-2k) mice. Quantitative cellular absorption of appropriate anti-Ia monoclonal antibodies and flow cytofluorometric analyses revealed that the B cell hybridomas examined herein expressed constitutively a number of surface I-Ak or I-Ek molecules that varied in an order of magnitude of 1 to 5. Such quantitative differences could be correlated precisely with (a) the capacity of B cell hybridomas to activate T cell clones to proliferate and/or to produce interleukin 2 in response to E beta k allodeterminant or to poly(Glu60Ala30Tyr10) presented in the context of I-Ak restriction element, and (b) the amount of monoclonal anti-I-Ak antibody required to inhibit antigen presentation to T cell clones. The possible implications of these data are discussed in the context of current models of regulation of Ia antigen expression by antigen-presenting cells.

Animals↗

PubMed1984

A rat anti-mouse T4 monoclonal antibody (H129.19) inhibits the proliferation of Ia-reactive T cell clones and delineates two phenotypically distinct (T4+, Lyt-2,3-, and T4-, Lyt-2,3+) subsets among anti-Ia cytolytic T cell clones.

Hybridoma H129 .19 was derived by fusion between spleen cells of a Lou / Ws1 rat immunized with an Lyt-1+,2- anti-I-Ak cytolytic T lymphocyte (CTL) clone and the nonsecreting myeloma X63-Ag8.653. The monoclonal antibody (mAb) H129 .19 (IgG2a, kappa) was selected for its capacity to inhibit the lytic potential of the immunizing clone. H129 .19 identified a monomorphic determinant on a 55 m.w. murine T cell differentiation antigen, which appeared to be homologous to the human T4 molecule in that: 1) H129 .19 reacted with 80% adult thymocytes, with a subset of splenic T cells, and with the interleukin 2 (IL 2)-producing EL4 thymoma; 2) The mAb bound to and inhibited the IL 2 production and the proliferation of various allo- or soluble antigen-reactive T cell clones that recognized restriction or activating determinants on the I-A or I-E molecules, respectively; 3) H129 .19 did not inhibit the proliferation and/or cytolysis of Lyt-2,3+ T cells specific for class I MHC antigen; and 4) Among six anti-Iak CTL clones examined in this study, the mAb H129 .19 reacted with two I-Ak-specific, Lyt-2,3- clones on which it exerted strong cytolysis inhibiting effect at the effector cell level. By contrast, two other anti-I-Ak and two anti-I-Ek CTL clones were found to express the Lyt-2,3+,T4- cell surface phenotype. The cytolytic potential of the latter clones was not inhibited by anti-Lyt-2,3 mAb. These studies strongly suggest that the mouse T4 molecule facilitates the recognition of class II MHC antigen by most but not all T cells.

Animals↗

PubMed1983

Induction of a cross-reactive idiotype dextran-positive antibody response in two IgH-Cb mouse strains treated with anti-J558 cross-reactive idiotype antibodies.

The effect of IdX-specific rabbit and allogeneic antiidiotype antibodies (Ab2) was investigated in vivo in Igh-Cb mouse strains with respect to the induction of a cross-reactive idiotype (IdX)-positive anti-alpha (1-3) Dextran (Dex) response. These C.B20 and C57Bl/6 mice have an allotype-linked incapacity to respond with IdX-positive anti-alpha (1-3) Dex antibodies upon conventional immunization with Dex B1355. 7 d after the rabbit Ab2 injections, IdX-positive Ig (Ab3) and IdX-positive anti-alpha (1-3) Dex antibodies (Ab1') were detected in the sera of each tested mouse. The affinity-purified Ab1' were idiotypically indistinguishable from reference BALB/c IdX-positive myeloma proteins and BALB/c anti-alpha (1-3) Dex antibodies (Ab1) in a competitive inhibition radioimmunoassay, while Ab3 Ig appeared idiotypically deficient and did not bind to Dex. The response to the alpha (1-6) linkage of Dex was not affected in these mice. A large fraction of the Ab1' and Ab3 responses of both mouse strains were of the IgG1 class. The Ab1' antibodies differed from BALB/c Ab1 by lower relative binding to five of eight tested Dex, and by expressing the Igh4b allotype determinants on the IgG1 antibodies. This study identifies the products of a VHDex gene that appears to be under regulatory control in the Ighb mice. Its association with the b haplotype suggests that this gene may differ structurally from the BALB/c VHDex gene.

Animals↗

PubMed1982

HLA and longevity.

One hundred fifty-five healthy nonagenarians, 45 men and 100 women, all French Caucasians, were phenotyped for alleles of the A, B, C, DR loci of the HLA complex. The observed HLA antigen frequencies were compared to those of a control series of 133 males and 179 females whose ages ranged from 10 to 50 years. When comparing the total young and elderly series, no significant differences were observed with respect to HLA antigen distribution or heterozygosity at any of the loci. When taking sex difference into account, however, an excess of the Cw1 antigen was found in the group of elderly females (p less than 0.001) and an excess of the Cw7 antigen in the group of elderly males (p less than 0.001). Of particular significance was the fact that Cw7 belonged in this instance to a phenotypic combination (and most probably to the corresponding haplotype) A1/Cw7/B8/DR3 which was found significantly increased in male nonagenarians (p less than 0.001). These results support the hypothesis that certain HLA haplotypes are associated with survival advantage.

Adolescent↗