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Accidental laser exposure to the eyes may result in serious visual impairment due to retina degeneration. Currently limited treatment is available for laser eye injury. In the current study, we investigated the therapeutic potential of bone marrow-derived stem cells (BMSCs) for laser-induced retinal trauma. Lineage negative bone marrow cells (Lin− BMCs) were labelled with quantum dots (Qdots) to track the cells in vivo. Lin− BMCs survived well after intravitreal injection. In vivo bromodeoxyuridine (BrdU) labelling showed these cells continued to proliferate and integrate into injured retinas. Furthermore, they expressed markers that distinguished retinal pigment epithelium (RPE), endothelium, pericytes and photoreceptors. Our results suggest that BMSCs participate in the repair of retinal lesions by differentiating into retinal cells. Intravitreal transplantation of BMSCs is a potential treatment for laser-induced retinal trauma.

T cells using the γδ T cell receptor (TCR) are abundant in mucosal and epidermal tissues in mice. Most studies of mucosal γδ T cells, however, have examined cells from the intestinal mucosa, whereas little is known about the presence or function of γδ T cells in the oral cavity. To better understand the involvement of oral γδ T cells in immunity, we have characterized TCR variable γ-gene usage in the buccal epithelium from normal mice, and from mice challenged locally with a non-replicating antigen (bovine serum albumin [BSA]) or by influenza-virus infection as a replicating antigen. Our findings demonstrate a restricted use of Vγ genes by buccal γδ T cells, consisting primarily of Vγ1.2, Vγ3, and Vγ5, with minimal use of Vγ2 and Vγ4 genes. Of particular interest, 3–4 days post-antigen challenge with BSA, there was a precipitous drop in the level of expression of Vγ1.2, Vγ3, and Vγ5 genes, and to a lesser extent for the Vγ2 gene, whereas Vγ4 gene expression increased between days 1 and 2 post-priming. In influenza-infected mice, a similar pattern was observed for the Vγ2 and Vγ5 genes, but not other Vγ genes. The immune-modulating effects of oral antigen exposure on buccal γδ T cells suggest that these cells are functionally involved in the local immune response to both replicating and non-replicating antigens in oral mucosal surfaces.

The thyroid hormones T(3) (tri-iodothyronine) and T(4) (thyroxine) are disseminated throughout the body via the circulation and are maintained across a range of physiological concentrations under the control of thyroid-stimulating hormone (TSH). T(3) (and T(4) after conversion to T(3)) influences many biological activities, including gene expression and protein synthesis, though little is known about the nature of pituitary-thyroid immune interactions. In the present study we show that serum T(3) and T(4) levels are sharply but transiently reduced during the first 24 h of systemic antigen exposure and that this is followed by suppressed levels of free T(4), after which there is rapid recovery to normal levels. Splenic dendritic cells, depending upon the stage of maturation/activation, were found to be a rich source of TSH, and CD11c(+) cells with dendritic cell morphology were present in the thyroid 1-3 days after antigen exposure. Moreover, antigen priming of hypophysectomized mice that are unable to make pituitary-derived TSH resulted in significant increases in circulating T(4), implying that compensation in the drop in thyroid hormones can be regulated from extrapituitary sources. These findings thus identify a novel set of immune-endocrine interactions that transpire during the early phase of antigen exposure, and they suggest that under appropriate conditions the immune system directly participates in the process of maintaining physiological homeostasis by contributing to the regulatory control of thyroid hormone activity.