Cooperative Roles of CTLA-4 and Regulatory T Cells in Tolerance to an Islet Cell Antigen

Adoptive transfer of ovalbumin (OVA)-specific T cells from the DO.11 TCR transgenic mouse on a Rag−/− background into mice expressing OVA in pancreatic islet cells induces acute insulitis and diabetes only if endogenous lymphocytes, including regulatory T cells, are removed. When wild-type OVA-specific/Rag−/− T cells, which are all CD25−, are transferred into islet antigen–expressing mice, peripheral immunization with OVA in adjuvant is needed to induce diabetes. In contrast, naive CTLA-4−/−/Rag−/− OVA-specific T cells (also CD25−) develop into Th1 effectors and induce disease upon recognition of the self-antigen alone. These results suggest that CTLA-4 functions to increase the activation threshold of autoreactive T cells, because in its absence self-antigen is sufficient to trigger autoimmunity without peripheral immunization. Further, CTLA-4 and regulatory T cells act cooperatively to maintain tolerance, indicating that the function of CTLA-4 is independent of regulatory cells, and deficiency of both is required to induce pathologic immune responses against the islet self-antigen

Registration of Four Jassid-Resistant Peanut Germplasm Lines: ICGV 86252, ICGV 86393, ICGV 86455, and ICGV 86462

Four elite peanut (Arachis hypogaea L.) germplasm lines, ICGV 86252 (Reg. no. GP-69, P1 585001), ICGV 86393 (Reg. no. GP-70, P1 585002), ICGV 86455 (Reg. no. GP-71, P1 585003), and ICGV 86462 (Reg. no. GP-72, P1 585004), resistant to jassid (Empoasca kerri Pruthi), were developed at the Asia Center of the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), Patancheru, India. They were released in 1993 by the ICRISAT Plant Materials Identification Committee

Registration of ICGV 86031 Peanut Germplasm

ICGV 86031 (Reg. no. GP-58, PI no. 561917) is a spanishtype peanut (Arachis hypogaea L. subsp. fastigiata Waldron var. vulgaris Hartz) developed at the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), Patancheru, India. It was released in 1991 by the Plant Materials Identification Committee of ICRISAT because of its resistance to thrips (Thripspalmi Karny), jassid (Empoasca kerri Pruthi), spodoptera [Spodoptera litura (Fabricius)], groundnut leaf miner (Aproaerema modicella Deventer) and bud necrosis virus (BNV), which causes bud necrosis disease (END) in peanut. ICGV 86031 has also been found to be photoperiod insensitive and resistant to iron deficiency chlorosis (4)

The Stress-Response Factor SigH Modulates the Interaction between Mycobacterium tuberculosis and Host Phagocytes

The Mycobacterium tuberculosis stress response factor SigH plays a crucial role in modulating the pathogen's response to heat, oxidative-stress, envelope damage and hypoxia. We hypothesized that the lack of this key stress response factor would alter the interaction between the pathogen and its host cells. We compared the interaction of Mtb, Mtb:Δ-sigH and a strain where the mutation had been genetically complemented (Mtb: Δ-sigH:CO) with primary rhesus macaque bone marrow derived macrophages (Rh-BMDMs). The expression of numerous inducible and homeostatic (CCL) β-chemokines and several apoptotic markers was induced to higher levels in the cells infected with Mtb:Δ-sigH, relative to Mtb or the complemented strain. The differential expression of these genes manifested into functional differences in chemotaxis and apoptosis in cells infected with these two strains. The mutant strain also exhibited reduced late-stage survival in Rh-BMDMs. We hypothesize that the product of one or more SigH-dependent genes may modulate the innate interaction of Mtb with host cells, effectively reducing the chemokine-mediated recruitment of immune effector cells, apoptosis of infected monocytes and enhancing the long-term survival and replication of the pathogen in this milieu The significantly higher induction of Prostaglandin Synthetase 2 (PTGS2 or COX2) in Rh-BMDMs infected with Mtb relative to Mtb: Δ-sigH may explain reduced apoptosis in Mtb-infected cells, as PTGS2 is known to inhibit p53-dependent apoptosis.The SigH-regulon modulates the innate interaction of Mtb with host phagocytes, perhaps as part of a strategy to limit its clearance and prolong its survival. The SigH regulon appears to be required to modulate innate immune responses directed against Mtb