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Proteomic dataset of Wt and PTPMT1 KO regulatory T cells

ABSTRACT: Mitochondrial defects are emerging as key drivers of gut inflammation, colitis, and IBD. Yet, their role in regulating immune tolerance, fine-tuned by helper T cells, is unclear. Understanding how metabolic changes in T cells impact gut tolerogenic mechanisms, including gut colonization and the balance between tolerance and disease, remains, therefore, a critical challenge. Here, we show that cardiolipin deficiency impairs tolerance to Helicobacter due to loss of regulatory T (Treg) cell function. Without cardiolipin, Treg cells lose metabolic fitness and immunosuppressive capacity igniting inflammation, particularly in the gut. Hence, mice with a T cell-specific deletion of the enzyme PTPMT1, essential for cardiolipin synthesis, are highly vulnerable to pathobiont infections even without microbiome imbalance. Notably, patients affected by Barth syndrome, a genetic disease characterized by severe cardiolipin deficiency, also exhibit inflammation and helper T cell imbalance. Overall, we found that cardiolipin in T cells preserves gut-immune homeostasis, dictating outcomes in pathobiont infections.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Regulatory T Cell

SUBMITTER: Proteomics Facility

LAB HEAD: Mauro Corrado

PROVIDER: PXD060518 | Pride | 2026-04-14

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	3259_using_MOUSEc_mbr_MC1_NoMod-lib.tsv.speclib	Tabular
	E2_ColID498_3259_01.raw	Raw
	E2_ColID498_3259_02.raw	Raw
	E2_ColID498_3259_03.raw	Raw
	E2_ColID498_3259_04.raw	Raw

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Proteomic dataset of Wt, PTPMT1 KO, CHOP KO and PTPMT1 CHOP double KO regulatory T cells

Project description:Mitochondrial defects are emerging as key drivers of gut inflammation, colitis, and IBD. Yet, their role in regulating immune tolerance, fine-tuned by helper T cells, is unclear. Understanding how metabolic changes in T cells impact gut tolerogenic mechanisms, including gut colonization and the balance between tolerance and disease, remains, therefore, a critical challenge. Here, we show that cardiolipin deficiency impairs tolerance to Helicobacter due to loss of regulatory T (Treg) cell function. Without cardiolipin, Treg cells lose metabolic fitness and immunosuppressive capacity igniting inflammation, particularly in the gut. Hence, mice with a T cell-specific deletion of the enzyme PTPMT1, essential for cardiolipin synthesis, are highly vulnerable to pathobiont infections even without microbiome imbalance. Notably, patients affected by Barth syndrome, a genetic disease characterized by severe cardiolipin deficiency, also exhibit inflammation and helper T cell imbalance. Overall, we found that cardiolipin in T cells preserves gut-immune homeostasis, dictating outcomes in pathobiont infections.

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