as it, for instance, inhibits the function of human CD8+ cancer-specific T cells. For example, this is the case of gallbladder cancer where BTLA+ CD8+ T cells are associated with inhibition of anticancer immunity. Similarly, BTLA+ CD8+ T cells show partial dysfunctionality and decrease secretion of IFN-γ in melanoma patients. Therefore, it seems that BTLA can be used as a novel antitumor therapy target. This notion is supported by the fact that in patients with hepatocarcinoma blocking of BTLA signalling increases the secretion of IFN-γ by CD8+ and CD4+ T cells. However, some studies have shown that, for instance, colorectal carcinoma is associated with lower BTLA expression and that the lower BTLA expression is connected with poor survival. Even in some cases of melanoma BTLA+ CD8+ lymphocytes are suggested to be connected with better outcomes of adoptive cell therapy. Hence, it seems that BTLA has rather a context-specific function. This fact should be taken into account if BTLA is to be used as a cancer therapy target. Infectious diseases As in the case of tumors, BTLA seems to be mainly an inhibitory molecule as, for instance, in the case of pulmonary tuberculosis where BTLA expression in CD4+ and CD8+ T cells is connected with the disease progression. Similar results can be seen during helminth infections. When mice are infected by Strongyloides ratti the mice with BTLA knockdown are faster at eliminating the parasite from the intestine probably through the production of IL-9. Furthermore, the course of virus infections seems to be negatively affected by BTLA as well. During chronic hepatitis B infection BTLA impairs T cell response and what's more blocking BTLA leads to T cell proliferation and higher cytokine production. However, as already mentioned in some cases BTLA seems to have a stimulatory role. This is the case of the aforementioned pulmonary tuberculosis where BTLA+ αβ T cells are predominantly of central memory phenotype and fight off Mycobacterium tuberculosis. A further example is an infection with vaccinia virus during which deletion of BTLA or HVEM causes instability and early apoptosis of CD8+ T cells. References Further reading External links Clusters of differentiation