TABLE 1.

Activation mechanisms and functional relevance of DURTs, NK cells, and ILCs in the context of mycobacterial infections

	HLA‐E–restricted T‐cells	MAIT cells	TCRγδ T‐cells	CD1‐restricted T cells		NK cells	ILCs
				Group 1 CD1‐restricted T‐cells	(i)NKT cells		ILC1s	ILC3s
Activation via antigen	Peptides:	Metabolic derivatives:	Phosphoantigens:	Lipids:		UL‐16–binding protein (ULBP)1
	self and pathogen‐derived	5‐OP‐RU	IPP, HMBPP, mGLP	GMM, MA, SGLs, GroMM	α‐GalCer, PIM
Activation via cytokines (TCR‐independent)		IL‐12/IL‐18			IL‐12/IL‐18	IL‐12/IL‐18	IL‐12/IL‐15/IL‐18	IL‐23
Functional relevance	Mtb growth inhibition	Recruitment to site of infection	Mtb growth inhibition	Mtb growth inhibition	Mtb growth inhibition	Mtb growth inhibition	IFN‐γ production	Th17 profile
	Cytotoxic, regulatory, and helper functions	Regulatory function	Cytotoxic function (perforin and granulysin)	Cytotoxic function (perforin, granzyme B, and granulysin)	Th1 and Th17 cytokine profiles	Trained immunity: IL‐1β, IL‐6, and TNF‐α production
	Th1 and Th2 cytokine profiled	Cytotoxic function (granzyme B)	IFN‐γ, GM‐CSF, IL‐3, TNF‐α production	Th1‐like cytokine profile		Regulatory function
			Immunoregulatory role (IL‐10)	CD40L, IFN‐γ, IL‐2, TNF‐α, and IL‐17a production		Cytotoxic function
			Th17 cytokine production			Memory‐like function
			Helper function			IFN‐γ production