Generation of early adaptive immune response is critical for the selective elimination of virus-infected cells and neutralization of viral antigens, thereby preventing the damage to the underlying lung parenchyma. Cytokines, chemokines, PAMPs, and DAMPs released by infected ATII and activated AMs in the lung are adequate to mount a well-coordinated and regulated adaptive immune response by priming lung resident DCs. After encountering the antigen-presenting DCs, naive CD4+ T cells differentiate into effector and memory CD4+ T cells. At least five different CD4+ T cell lineages are known (TH1, TH2, TH17, TFH, and TREG cells) with prominent roles of TH1 and TFH cells in mounting antiviral response during SARS-CoV infection (Channappanavar et al., 2014). Additionally, some studies have also shown a functional TH2 response in PBMCs derived from COVID-19 patients. Release of TH2 specific cytokines like IL-4 and IL-5 was observed in vitro after these cells were stimulated (Weiskopf et al., 2020). Similarly, these patients show enhanced production of IL-17 along with other TH17 cell-specific cytokines (Liu J. et al., 2020; Wu and Yang, 2020). These findings suggest that the TH cell response in COVID-19 patients is complex concerning other infections, and this complexity may partly depend upon the prevailing pathophysiological state of a patient.