Epidermal γδ T cells sense precancerous cellular dysregulation and initiate immune responses

Hyperplasia associated with a loss of tissue homeostasis can induce DNA replication stress, leading to precancerous dysregulation. Epidermal γδ T cells reside in the primary barrier that protects against diverse environmental insults; however, the functions of these T cells in tissue surveillance are not completely understood. In mice with inducible Notch1 inactivation in keratinocytes that causes epidermal hyperplasia, epidermal γδ T cells sensed stressed keratinocytes and migrated into the cutaneous draining lymph nodes. Simultaneous induction of β-galactosidase (β-Gal) as a putative antigen expressed in the process of precancerous dysregulation and Notch1 ablation in the epidermis resulted in elevated β-Gal-specific IgG2a production. Epidermal γδ T cells were found to have the capacity to express chemokine (C-C motif) receptor 7 and migrate into the lymph nodes. Cutaneous draining lymph node cells in Notch1-inactivated mice expressed high levels of IFN-γ upon anti-CD3 plus anti-CD28 stimulation. Furthermore, induced expression of β-Gal in mice that lacked epidermal γδ T cells failed to induce anti-β-Gal IgG. These results suggest that epidermal γδ T cells play an essential role in the initiation process of epidermal antigen-specific humoral immune responses and demonstrate the importance of epidermal γδ T cells in sensing precancerous dysregulation and activating adaptive immunit

Karyotypical characteristics of two allopatric African populations of anhydrobiotic Polypedilum Kieffer, 1912 (Diptera, Chironomidae) originating from Nigeria and Malawi

The African chironomid Polypedilum vanderplanki Hinton, 1951 is the only chironomid able to withstand almost complete desiccation in an ametabolic state known as anhydrobiosis. The karyotypes of two allopatric populations of this anhydrobiotic chironomid, one from Nigeria and another from Malawi, were described according to the polytene giant chromosomes. The karyotype from the Nigerian population was presented as the reference chromosome map for P. vanderplanki. Both populations, Nigerian and Malawian, showed the same number of chromosomes (2n=8), but important differences were found in the band sequences of polytene chromosomes, and in the number and the arrangement of active regions between the two populations. Such important differences raise the possibility that the Malawian population could constitute a distinct new species of anhydrobiotic chironomid

Epidermal {gamma}{delta} T cells sense precancerous cellular dysregulation and initiate immune responses

Hyperplasia associated with a loss of tissue homeostasis can induce DNA replication stress, leading to precancerous dysregulation. Epidermal {gamma}{delta} T cells reside in the primary barrier that protects against diverse environmental insults; however, the functions of these T cells in tissue surveillance are not completely understood. In mice with inducible Notch1 inactivation in keratinocytes that causes epidermal hyperplasia, epidermal {gamma}{delta} T cells sensed stressed keratinocytes and migrated into the cutaneous draining lymph nodes. Simultaneous induction of β-galactosidase (β-Gal) as a putative antigen expressed in the process of precancerous dysregulation and Notch1 ablation in the epidermis resulted in elevated β-Gal-specific IgG2a production. Epidermal {gamma}{delta} T cells were found to have the capacity to express chemokine (C-C motif) receptor 7 and migrate into the lymph nodes. Cutaneous draining lymph node cells in Notch1-inactivated mice expressed high levels of IFN-{gamma} upon anti-CD3 plus anti-CD28 stimulation. Furthermore, induced expression of β-Gal in mice that lacked epidermal {gamma}{delta} T cells failed to induce anti-β-Gal IgG. These results suggest that epidermal {gamma}{delta} T cells play an essential role in the initiation process of epidermal antigen-specific humoral immune responses and demonstrate the importance of epidermal {gamma}{delta} T cells in sensing precancerous dysregulation and activating adaptive immunity

Alteration of Immune Responses by N-acetylglucosaminyltransferase V during Allergic Airway Inflammation

Background: p-1,6-N-acetylglucosaminyltransferase V (Mgat5 or GlcNac-TV), which is involved in the glyco- sylation of proteins, is known to be important for down-regulation of TCR-mediated T-cell activation and negatively regulates induction of contact dermatitis and experimental autoimmune encephalomyelitis. However, the role of Mgat5 in the induction of allergic airway inflammation remains unclear. Methods: To elucidate the role of Mgat5 in the pathogenesis of allergic airway inflammation, ovalbumin (OVA)-induced airway inflammation was induced in Mgat5-deficient mice. The OVA-specific lymphocyte proliferation and cytokine production levels, OVA-specific IgG1, IgG2a and IgE levels in the serum, and the number of leukocytes and cytokine levels in the bronchoalveolar lavage (BAL) fluid were compared between wild-type and Mgat5-deficient mice. Results: OVA-specific lymphocyte proliferation and production of IFN-y and IL-10, but not IL-4, were increased in Mgat5-deficient mice, suggesting that Th2-type immune responses are seemed to be suppressed by increased IFN-y and IL-10 production in these mice. However, Th2-type responses such as OVA-specific IgG1, but not IgE, and IL-5 levels in BAL fluids were increased in Mgat5-deficient mice. Meanwhile, the number of eosinophils was normal, but the numbers of neutrophils, macrophages and lymphocytes were reduced, in these mutant mice during OVA-induced airway inflammation. Conclusions: Mgat5-dependent glycosylation of proteins can modulate acquired immune responses, but it is not essential for the development of OVA-induced eosinophilic airway inflammation

IL-25, IL-33 and TSLP receptor are not critical for development of experimental murine malaria

IL-25, IL-33 and TSLP, which are produced predominantly by epithelial cells, can induce production of Th2-type cytokines such as IL-4, IL-5 and/or IL-13 by various types of cells, suggesting their involvement in induction of Th2-type cytokine-associated immune responses. It is known that Th2-type cytokines contribute to host defense against malaria parasite infection in mice. However, the roles of IL-25, IL-33 and TSLP in malaria parasite infection remain unclear. Thus, to elucidate this, we infected wild-type, IL-25−/−, IL-33−/− and TSLP receptor (TSLPR)−/− mice with Plasmodium berghei (P. berghei) ANKA, a murine malaria strain. The expression levels of IL-25, IL-33 and TSLP mRNA were changed in the brain, liver, lung and spleen of wild-type mice after infection, suggesting that these cytokines are involved in host defense against P. berghei ANKA. However, the incidence of parasitemia and survival in the mutant mice were comparable to in the wild-type mice. These findings indicate that IL-25, IL-33 and TSLP are not critical for host defense against P. berghei ANKA