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Dissecting the intrinsic role of SLC4A2 in the development of liver inflammation in a mouse model of PBC

Award Number: R03AI196747
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/02/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2027

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Dissecting the intrinsic role of SLC4A2 in the development of liver inflammation in a mouse model of PBC - Project Summary/Abstract The SLC4A2 (or Anion Exchanger2, AE2) is a ubiquitous membrane transporter that mediates the sodium (Na+)- independent and electroneutral exchange of chloride (Cl−) and bicarbonate (HCO3−) ions, and participates in the regulation of intracellular pH (pHi). AE2-deficiency in humans has been linked with the development of Primary Biliary Cholangitis (PBC), which is a chronic cholestatic liver disease associated with autoimmune phenomena. Supporting these findings, mice with whole-body deletion of SLC4A2 develop a spontaneous and progressive autoimmune cholangitis that resembles the human PBC. However, the cell intrinsic requirement of SLC4A2 in immune cells and/or biliary epithelial cells and the mechanisms underlying the loss of tolerance against biliary epithelial cells in the absence of SLC4A2 are unknown. Here, we aim to dissect the role of SLC4A2 in the development of liver inflammation and autoimmune cholangitis using SLC4A2 conditional knockout (cKO) mice. To this end, we have generated tissue-specific SLC4A2-cKO in the liver (i.e., Slc4a2fl/flAlbCre+ mice) as well as in T cells (i.e., Slc4a2fl/flCd4Cre+ mice) to study the requirement of this membrane transporter in immune tolerance in the liver. We aim to: 1) characterize the immune cell composition in the liver and lymphoid organs of Slc4a2fl/flCd4Cre+, Slc4a2fl/flAlbCre+ mice and their control littermates, and ii) study the alterations that occur in T cells and liver cells in the absence of SLC4A2. Investigating the mechanisms underlying the autoimmune cholangitis and liver inflammation caused by SLC4A2 deficiency in mice will be an important step forward to better understand the etiopathogenesis of PBC and to the development of future therapeutic approaches to treat these patients.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $164,000 )
2026	2026	UNIVERSITY OF CHICAGO	5801 S ELLIS AVE	CHICAGO	IL	60637	COOK	USA	Allergy and Infectious Diseases Research	000	1	4/2/2026	NEW	$164,000
														Subtotal = $164,000

Grand Total All Awards = $164,000

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Dissecting the intrinsic role of SLC4A2 in the development of liver inflammation in a mouse model of PBC

Award Number: R03AI196747

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 04/02/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2027

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