Leishmaniasis is a complex infectious parasitic disease caused by protozoa of the genus Leishmania, belonging to a group of neglected tropical diseases. It establishes significant global health challenges, particularly in socio-economically disadvantaged regions. Macrophages, as innate immune cells, play a crucial role in initiating the inflammatory response against the pathogens responsible for this disease. Macrophage polarization, the process of differentiating macrophages into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes, is essential for the immune response in leishmaniasis. The M1 phenotype is associated with resistance to Leishmania infection, while the M2 phenotype is predominant in susceptible environments. Notably, various immune cells, including T cells, play a significant role in modulating macrophage polarization by releasing cytokines that influence macrophage maturation and function. Furthermore, other immune cells can also impact macrophage polarization in a T-cell-independent manner. Therefore, this review comprehensively examines macrophage polarization’s role in leishmaniasis and other immune cells’ potential involvement in this intricate process.

Mycobacterium tuberculosis complex causes tuberculosis (TB), a disease that causes pulmonary inflammation but can also affect other tissues. Despite macrophages having a defined role in TB immunopathogenesis, other innate immune cells, such as neutrophils, are involved in this process. These cells have high phagocytic ability and a microbial-killing machine comprised of enzymes, antimicrobial peptides, and reactive oxygen species. In the last two decades, a new neutrophil immune response, the neutrophil extracellular traps (NETs), has been intensely researched. NETs comprise DNA associated with histones, enzymes, and antimicrobial peptides. These structures are related to antimicrobial immune response and some immuno-pathogenesis mechanisms. This mini review highlights the role of NETs in tuberculosis and how they can be helpful as a diagnostic tool and/or therapeutic target.

Many studies have focused on SARS-CoV-2 and Mycobacterium tuberculosis (Mtb) co-infection consequences. However, after a vaccination plan against COVID-19, the cases of severe disease and death are consistently controlled, although cases of asymptomatic and mild COVID-19 still happen together with tuberculosis (TB) cases. Thus, in this context, we sought to compare the T cell response of COVID-19-non-vaccinated and -vaccinated patients with active tuberculosis exposed to SARS-CoV-2 antigens. Flow cytometry was used to analyze activation markers (i.e., CD69 and CD137) and cytokines (IFN-γ, TNFα, IL-17, and IL-10) levels in CD4⁺ and CD8⁺ T cells upon exposure to SARS-CoV-2 peptides. The data obtained showed that CD8⁺ T cells from non-vaccinated TB patients present a high frequency of CD69 and TNF-α after viral challenge compared to vaccinated TB donors. Conversely, CD4⁺ T cells from vaccinated TB patients show a high frequency of IL-10 after spike peptide stimulus compared to non-vaccinated patients. No differences were observed in the other parameters analyzed. The results suggest that this reduced immune balance in coinfected individuals may have consequences for pathogen control, necessitating further research to understand its impact on clinical outcomes after COVID-19 vaccination in those with concurrent SARS-CoV-2 and Mtb infections.