Secreted and transmembrane protein 1B (Sectm1b) is a gene product that, along with Sectm1A, is involved in modulating T-cell activation. It binds strongly to CD7, like Sectm1A, and can compete with Sectm1A for CD7 binding [1]. While Sectm1A acts as a co-stimulator of T cells, enhancing IL-2 production and proliferation, Sectm1B proves inhibitory to TCR-mediated T cell activation, and both functional outcomes are CD7-independent, suggesting the existence of alternative receptors for both ligands [1].

In the context of pneumococcal pneumonia, Sectm1a and Sectm1b were identified as highly expressed secreted products in airway epithelial cells during infection. Sectm1 was induced during the early stages of pneumococcal pneumonia, and type I IFN signaling was necessary and sufficient for its induction in lung epithelial cells [2]. Although the references do not mention Sectm1b-specific KO/CKO mouse models, Sectm1a was shown to bind to myeloid cells, especially Ly6G(bright)CD11b(bright) neutrophils in the infected lung, and increase the expression of the neutrophil-attracting chemokine CXCL2 by these neutrophils [2].

In summary, Sectm1b plays a role in inhibiting TCR-mediated T-cell activation, potentially through alternative receptors. In the context of pneumococcal pneumonia, the Sectm1 genes (including Sectm1b) are induced in airway epithelial cells via type I IFN signaling. While direct evidence from Sectm1b KO/CKO mouse models is lacking in the provided references, the overall findings suggest its importance in immunological regulation, both in T-cell modulation and in the response to pneumococcal pneumonia.