Contributes to systemic listeriosis in mice by decreasing host IL-6 cytokine production and thus evasion of the host immune response. Does not contribute to invasion of the host intestinal tissue. In the absence of SrtA in exponential phase some protein is still anchored to the cell wall while protein levels are the same in the srtA mutant; in stationary phase much less protein accumulates (PubMed:22837151). During exponential growth detected on the cell surface as a series of dots in a helical pattern, it is excluded from the septum (PubMed:21725001). The helical pattern of InlA does not overlap with that of InlH, InlJ or Hbp2 (SvpA) (PubMed:21725001). In stationary phase colocalizes with InlA at cell poles and at the septum, the location shift requires SigB (PubMed:21725001). More prevalent in stationary than exponential phase (at protein level) (PubMed:21725001, PubMed:20176794). Single gene transcripts are substantially decreased in a sigB mutant, induced in mouse gut (PubMed:20176794). Induced as cells approach stationary phase and by growth at pH 5.5, at 45 degrees Celsius, in 7.5% NaCl and by oxidative stress (at protein level) (PubMed:20176794, PubMed:21725001). The N-terminus (36-79) resembles a truncated EF hand, the LRR region (80-262) has a curved form while residues 263-343 form an Ig-like region. Increased expression of InlA (PubMed:20176794). No change in invasion or bacterial survival in host mamammalian cells including macrophages (PubMed:20176794). Decreased bacterial counts in blood, spleen and liver of intravenously inoculated BALB/c and C57BL/6 mice (PubMed:20176794, PubMed:11575932). Increased production of host IL-6 in liver and spleen of intravenously infected BALB/c mice, but not in macrophage cell lines (PubMed:20176794). Belongs to the internalin family.