Tryptophan aspartate-containing coat protein (CORO1A) suppresses Toll-like receptor signalling in Mycobacterium leprae infection.

Mycobacterium leprae is an intracellular pathogen that survives within the phagosome of host macrophages. Several host factors are involved in producing tolerance, while others are responsible for killing the mycobacterium. Tryptophan aspartate-containing coat protein (TACO; also known as CORO1A or coronin-1) inhibits the phagosome maturation that allows intracellular parasitization. In addition, the Toll-like receptor (TLR) activates the innate immune response. Both CORO1A and TLR-2 co-localize on the phagosomal membrane in the dermal lesions of patients with lepromatous leprosy. Therefore, we hypothesized that CORO1A and TLR-2 might interact functionally. This hypothesis was tested by investigating the effect of CORO1A in TLR-2-mediated signalling and, inversely, the effect of TLR-2-mediated signalling on CORO1A expression. We found that CORO1A suppresses TLR-mediated signal activation in human macrophages, and that TLR2-mediated activation of the innate immune response resulted in suppression of CORO1A expression. However, M. leprae infection inhibited the TLR-2-mediated CORO1A suppression and nuclear factor-kappaB activation. These results suggest that the balance between TLR-2-mediated signalling and CORO1A expression will be key in determining the fate of M. leprae following infection.

A histological study of the eye lesions in 12 leprosy patients with tuberculoid lesion in 4 eyes.

The histological reactions in 12 eyes of 12 leprosy patients were studied (5 BT, 1 BB, 1 BL and 5 LL). Granuloma lesions composed of epithelioid cells, Langerhans giant cells, macrophages and lymphocytes were found in various intraocular tissues, e.g. cornea, sclera, iris, ciliary body or retina in 4 patients (1 BT and 3 LL). Of the 3 LL patients, according to the records, 2 were cured and in the other patient the outcome of the treatment was not mentioned. In view of the finding of the granulomatous lesions in the clinically cured patients and tuberculoid granuloma in the intraocular tissues in the LL patients, could there be some peculiarities in the intraocular sites? Or perhaps the tuberculoid reaction is just a manifestation of an upgrading reaction? More examinations on human leprosy eye specimens will be needed to answer these questions.