Immunosuppressive factor(s) specific for L-glutamic acid(50)-L- tyrosine(50) (GT). II. Presence of I-J determinants on the GT-suppressive factor

The responses to the synthetic antigens, L-glutamic acid(60)-L- alanine(30)-L-tyrosine(10) (GAT) and L-glutamic acid(50)-L-tyrosine(50) (GT) are controlled by genes in the I region of the mouse H-2 complex (1-3). Preimmunization of the mice bearing the H-2(p,q,s) nonresponder haplotypes with GAT stimulates the development of suppressor T cells that inhibit in vivo or in vitro antibody responses to GAT complexed to the immunogenic carrier, methylated bovine serum albumin (GAT-MBSA) (4). The copolymer GT is not immunogenic in any inbred mouse strain tested, and has a suppressive effect on the antibody responses to GT-MBSA in mouse strains bearing the H-2(d,f,k,s) haplotypes; suppressor T cells have been demonstrated to be responsible for specific GT suppression (3). We have obtained specific suppressive extracts from thymus and spleen cells of GAT-or GT-primed suppressor strains (5,6). The specific suppressive T-cell factors in the active extracts have been characterized (6,7) and appear similar to the carrier-specific suppressor factor described by Tada and Taniguchi (8). These products belong to a family of newly identified molecules coded for by the I region of the H-2 complex with affinity for antigen and helper (9,10) or suppressive (5-8) regulatory activity on the immune response. Recently, Tada et al. have reported that the keyhole limpet hemocyanin (KLH)-specific suppressor factor is coded for by the I-J subregion of the H-2 complex (11). We now demonstrate also that a GT-specific suppressor factor extracted from the spleens and thymuses of B10.BR (H-2(k)) mice bears determinants controlled by the I-J subregion of the H-2 complex

Etude Clinique des niveaux de perturbation de la metacognition, de la cognition sociale et du contrôle exécutif dans la pathologie frontale

Recent and convergent studies in neuropsychology have suggested the importance of frontal regions to the integrity of a number of functions such as metamemory capacities, executive functions, and social skills (Theory of Mind : ToM). In this original work, following Stuss et Anderson (2004), we assume a link between disturbances of these functions. We proposed to 16 frontal patients and 20 matched healthy subjects a protocol designed to test metamemory, ToM and executive functions in order to analyze the relations between disturbances of self-awareness (metamemory) and awareness of others (ToM), and cognitive control (executive functions). Our results confirm the importance of frontal lobes on these capacities. No correlation was found between measures of metamemory, measures of ToM and executive scores. The observation of individual profiles emphasizes the existence of dissociations between self awareness and consciousness of the others, and between these two forms of metacognitive control and the executive functioning. These results confirm the importance to engage more studies combining aspects of ToM, metacognition and executive control, to better understand the organization and architecture of the functions supported by frontal lobe

Genomic epidemiology reveals multiple introductions of Zika virus into the United States

Zika virus (ZIKV) is causing an unprecedented epidemic linked to severe congenital abnormalities. In July 2016, mosquito-borne ZIKV transmission was reported in the continental United States; since then, hundreds of locally acquired infections have been reported in Florida. To gain insights into the timing, source, and likely route(s) of ZIKV introduction, we tracked the virus from its first detection in Florida by sequencing ZIKV genomes from infected patients and Aedes aegypti mosquitoes. We show that at least 4 introductions, but potentially as many as 40, contributed to the outbreak in Florida and that local transmission is likely to have started in the spring of 2016-several months before its initial detection. By analysing surveillance and genetic data, we show that ZIKV moved among transmission zones in Miami. Our analyses show that most introductions were linked to the Caribbean, a finding corroborated by the high incidence rates and traffic volumes from the region into the Miami area. Our study provides an understanding of how ZIKV initiates transmission in new regions

VH gene-family representation in peripheral activated B cells from systemic lupus erythematosus (SLE) patients

A semiquantitative polymerase chain reaction (PCR) assay described in this study has been used to analyse the VH1, VH3 and VH4 repertoire expressed by total IgM+ and IgG+ B cells from normal individuals and lupus patients. This approach consists of a combination of B cell selection, utilization of the anchored PCR technique to avoid technical bias in the amplification of different VH gene family cDNA templates, and screening of the amplified IgM or IgG cDNA rearrangements by family-specific oligonucleotide probes. In four lupus patients, VH family representation in IgM+ and IgG+ in vivo activated B cells, selected by anti-CD71 antibody, and in total CD19+ B cells were compared. In all patients, VH4 gene family segments were preferentially underrepresented in IgM+ activated B cells. In IgG+ B cells the results suggest that VH4 expression is variable, depending on the phase of the disease. Polyclonal B cell activation, which is usually considered as being the first event in autoantibody production in SLE, cannot explain our results. The data evoke the possible involvement of a VH4-specific B cell superantigen in the onset or development of SLE. This hypothesis is also supported by the sequence conservation of the fourth β loop—a putative superantigen binding site—of functional VH4 gene segments which are preferentially used by anti-dsDNA lupus antibodies of established clones and hybridomas