Effect of Treg on immunopathology or pathogen load


Helicobacter pylori

Treg expand in mucosa, CD25 depletion reduces bacterial burden but generates pathology and inflammation.

Treg depletion does not influence bacterial colonization or immunopathology

[32] [33]


Herpes simplex virus

Treg ablation generates CD8 T cell response with an efficient viral clearance.

Treg depletion associates with exacerbated viral burden in mucosa and nervous system.



Mycobacterium tuberculosis

Treg depleted mice show decreased bacterial burden in the lungs with pathogen specific effector T cells.

Co-transfer of Treg with Th into RAG-1-deficient mice results in suppression of effector CD4 T cells, responsible for protection

Pathogen-specific Tregs activated




Leishmania major

Treg accumulate in the dermis, suppress the ability of effector cells to clear parasite and provide long-term protection from re-infection.


West nile virus

Treg expand in lymphoid organs and allow memory formation through promoting antigen persistence. Treg-deficient mice have impaired number of memory CD8 T cells


Trichuris muris

Early Treg depletion accelerates worm clearance with reduced Th1 mediated inflammation. However, the worm titre is augmented when Treg are depleted following infection.


Salmonella typhimurium

Depletion of Treg early after infection accelerates bacterial eradication. However, depletion during later phase is associated with no significant changes in bacterial clearance.


Retroviral infection

Transient ablation of Treg following a chronic retroviral infection helps CD8 T cells to recover antiviral potency.


Friend virus

Depletion of Treg results in a significant increase of FV-specific CD8 T-cell mediated responses which diminishes FV loads in lymphatic organs

[44] [45]

Hepatitis C virus

Hepatitis C virus induces Treg to exert their suppressive potency on effector T cells and promotes HCV persistence


Respiratory syncytial virus

Treg rapidly accumulates in draining LNs and lungs

Depletion of Treg results delayed viral clearance, aggravated disease intensity, including enhanced weight loss, airway restriction and morbidity.

Augmented weight loss with delayed recovery following ablation of Treg.

[50] [51]



Leishmania panamensis

Depletion of Tregs results increased parasite load, enlarged lesions, and enhanced production of IL-17 and IFN-γ. Adoptive transfer of Tregs halts disease progression, lowers parasite burden, and reduces cytokine production.