Mycobacterium tuberculosis is a major human pathogen and the existing tuberculosis (TB) vaccine, BCG, is ineffective at preventing its transmission. Understanding the immunological characteristics of protective immunity is essential for the rational design of improved TB vaccines. We have shown pulmonary immunisation with two novel vaccines, the recombinant influenza A virus (rIAV) PR8.p25 and the M. tuberculosis fusion protein-adjuvant vaccine, CysVac2-Advax, is protective against M. tuberculosis in mice. This protective immunity is associated with the development of M. tuberculosis antigen-specific CD4+ resident memory T cells (TRM) in the lungs, which protect against TB by rapidly responding to pathogen exposure. Genes involved in the formation and effector functions of CD4+ TRM are poorly understood. To characterise differences in gene expression of pulmonary vaccine-induced TRM, we adoptively transferred into C57BL/6 mice TCR-transgenic CD4+ T cells specific for IAb-restricted p25 peptide, present in both vaccines, and immunised them with either vaccine by the pulmonary route. After six weeks, we isolated p25-specific CD4+ TRM from the lungs by FACS sorting, and measured their gene expression profiles with the Nanostring™ immunology panel supplemented by genes associated with TRM. TRM induced by rIAV showed differential expression of 238 genes compared with naïve T cells, of which 43 were also differentially regulated compared to effector and effector memory T cells. Principal component analysis showed that they differed from these T cell populations in their upregulation of many genes, including chemokine receptors, transcription factors and effector molecules. TRM induced by CysVac2-Advax shared an overlapping gene expression profile to rIAV-induced TRM, with both groups upregulating chemokine receptors and effector genes. CysVac2-Advax TRM uniquely elevated expression of genes related to Th17 differentiation, while rIAV TRM upregulated other transcription factors and effector genes. Therefore, TRM induced by both vaccines protect against M. tuberculosis, but through distinct effector mechanisms.