Premières données sur les Halictidae (Hymenoptera : Apoidea) de la région de Batna (Est algérien)

First data about Halictidae (Hymenoptera: Apoidea) in the región of Batna (Eastern Algeria) Investigations carried out on Halictidae bees in different localities in the region of Batna during the spring and summer seasons of 2009 and 2012 allowed the identification of 35 species; Lasioglossum musculum is reported for the first time in Algeria. The presence of Sphecodes puncticeps Thomson, 1870, a cleptoparasitic species, is confirmed. The flowers visited and the flight period of each species are noted.     

Immunogenic Ia-binding peptides immobilize the Ia molecule and facilitate its aggregation on the B cell membrane. Control by the M1s-1 gene

Aggregation (e.g., through cross-linkage) of cell surface molecules is in various biologic systems a necessary event in cellular activation. Examining the Ia molecule on B cells we found that aggregation is a function of the surface Ag mobility; the higher the fraction of immobile molecules on the plane of the membrane, the better Ia forms aggregates and patches. We identify two factors that control Ia mobility and aggregability. One factor is the M1s-1a gene product; the other factor is an Ia-reactive immunogenic peptide. Both factors increase Ia aggregability and reduce the MHC Ag mobility.     

A stimulatory Mls-1 superantigen is destroyed by ultraviolet light while other Mtv-7 antigens remain intact. Significance for Mls-1 unresponsiveness.

Accessory cells present Ag together with costimulatory signals as immunogens and without costimulatory signals as tolerogens. Responsiveness and unresponsiveness are thus alternatives of T cell immune reactions to Ag. Superantigens appear to make an exception; being presented by accessory cells capable of providing costimulatory signals, these Ag induce a strong T cell response but leave T cells unresponsive to a secondary challenge (anergy). We show here that T cell anergy is not a mandatory consequence of superantigen-induced activation. Mls-1- BALB/c recipients of DBA/2 spleen cells mount vigorous Mls-1 responses in vivo but their T cells retain the ability to respond to a subsequent Mls-1 challenge in vitro. We tested the possibility that the inability of DBA/2 spleen cells to inactivate Mls-1-reactive BALB/c T cells was the result of excessive costimulatory activity provided by Mls-1+ DBA/2 B cells. Costimulatory accessory cell activity has been reported to be destroyed by UV light. We exposed superantigen-presenting cells to UV radiation and found that they had lost the ability to stimulate an Mls-1 response without, however, gaining the capacity to render Mls-1-specific T cells anergic. Despite their inability to noticeably stimulate Mls-1-reactive T cells, UV-treated Mls-1+ lymphocytes induced an absolute unresponsiveness in Mls-1- recipients to a second challenge with the superantigen. Our data are in agreement with previous evidence, confirmed here, that BALB/c mice establish immunity against Mls-1+ cells, which causes the accelerated rejection of superantigen-bearing lymphocytes. Thus, our data imply that, whereas it takes stimulatory superantigenic Mtv-7 gene products to induce the activation of superantigen-reactive T cells, nonsuperantigenic Mtv-7 gene products may induce an immune response leading to the elimination of Mtv-7+ lymphoid cells.