Influenza A viruses pose a significant pandemic threat, with H2N3 in particular representing a subtype of particular concern due to limited population immunity and potential for zoonotic transmission. Traditional antibody-centric vaccine strategies face fundamental limitations stemming from antigenic drift and shift in hemagglutinin and neuraminidase surface proteins, necessitating annual reformulation and demonstrating reduced efficacy against mismatched strains. T-cell-mediated immunity offers a complementary approach by targeting highly conserved internal viral proteins such as nucleoprotein and matrix protein 1, thereby enabling cross-subtype protection independent of surface antigen variability. This review systematically examines the role of CD8?+?cytotoxic T lymphocytes, CD4?+?helper T cells, and tissue-resident memory T cells in controlling H2N3 influenza infection, with particular emphasis on mechanisms underlying heterosubtypic immunity. Evidence from preclinical models and human cohort studies demonstrates that pre-existing T-cell responses correlate with reduced disease severity across antigenically diverse influenza strains, even in the absence of strain-specific neutralizing antibodies. Recent advances in vaccine platforms—including viral vectors, mRNA technologies, and epitope-based approaches—show promise for inducing robust T-cell responses targeting conserved epitopes. Systems immunology and artificial intelligence-assisted epitope prediction are revolutionizing vaccine design by identifying pan-HLA-restricted epitopes with broad population coverage. However, significant challenges persist, including HLA diversity, immune senescence, absence of validated correlates of protection, and regulatory uncertainties. Collectively, this review demonstrates that integration of humoral and cellular immunity through combination vaccine strategies is essential for advancing universal influenza vaccines capable of providing durable, cross-protective immunity against both seasonal and pandemic strains, including re-emerging H2-like viruses.