Here, we expand on this finding by demonstrating that BTLA was not only upregulated on mouse lymphocytes and contributed to cellular apoptosis in primary and secondary lymphoid organs that associated with CD4+ T-cell and B-cell loss, but also that BTLA was seen at a higher frequency on CD4+ lymphocytes in the SIRS patients that developed subsequent infections. The gene discussed is BTLA; the disease is systemic inflammatory response syndrome.