Balb c h 2d mice

C57BL/6 (wild type and T-bet^−/−, H-2^b) and BALB/c mice (H-2^d) aged 10-12 weeks were purchased from The Jackson Laboratory (Bar Harbor, ME). Foxp3-GFP(22 (link)) and TEa T cell receptor (TCR) transgenic(23 (link)) mice on a C57BL/6 background were from A. Rudensky (Memorial Sloan Kettering Cancer Center, NY, NY). The TEa TCR transgene recognizes I-E^d peptide presented by I-A^b. Eomes^−/− (24 (link)) mice on a C57BL/6 background were from A. Banerjee (University of Maryland, Baltimore, MD). T-bet^−/− mice were crossed with Foxp3-GFP mice to generate T-bet^−/− Foxp3-GFP transgenic mice. All experiments were performed with age- and sex-matched mice in accordance with Institutional Animal Care and Utilization Committee approved protocols.

Young (2–4 months) C57BL/6 (H2^b), aged (16–18 months), and advanced aged (22–24 months) C57BL/6 mice were obtained from the National Institutes of Aging rodent colony. Young donor BALB/c mice (H2^d) and C57BL/6 CD45.1⁺ were purchased from the Jackson Laboratory (Bar Harbor, ME, USA).
Full-thickness BALB/c skin was transplanted to the dorsum of C57BL/6 recipients as described previously [30 (link)]. Recipients were treated with anti-CD45RB (clone HB220, 100 µg intraperitoneally on days −1, 0, 1, 2, 5, and 8 relative to transplantation) and anti-CD154 (clone MR1, 250 µg intraperitoneally on days 0, 2, 6, and 8 relative to transplantation). Both antibodies were purchased from BioXcell (Lebanon, NH, USA). Complete loss of the skin graft area was considered as rejection. B cell depletion was accomplished using an anti-CD20 monoclonal antibody (four doses of 100 µg/dose administered on days −5, +5, +15, and +25 relative to transplantation). The anti-CD20 antibody (clone 5D2) was obtained from Genentech (San Francisco, CA, USA).
The Yale University Institutional Animal Care and Use Committee approved the use of animals in this study.

Pgam5^-/- mice have previously been described(Lu et al., 2014 (link)). Male BALB/c (H-2^d) mice were purchased from Jackson laboratories. WT and Pgam5^-/- mice were on C57BL/6 background (H-2^b). 6-8 week old male littermates were used for the experiments. All mice were bred and housed in the specific pathogen-free facility at the Skirball Institute of Biomolecular Medicine and used in accordance with institutional guidelines.

We utilized wild type (WT) C57BL/6 (H2^b) and Balb/C (H2^d) mice (The Jackson Laboratory, Bar Harbor, ME) as well as a C57BL/6 mouse strain with a T cell-specific defect in TGFβ signaling (Cd4-TGFBR2 (Jackson Laboratories #005551; also named TGFβ receptor II dominant negative (TGFβ RII DN)) (H2^b)(29 (link)). Five to six week old Balb/C mice were inoculated with 150 H. polygyrus third stage larvae (L3) by oral gavage. Infective H. polygyrus L3 (original specimens archived at the U.S. National Helminthological Collection no. 81930; also named H. polygyrus (bakeri) or H. bakeri in some publications (30 (link), 31 (link)) were obtained from mouse fecal cultures of eggs by the modified Baermann method and stored at 4°C until used. The number of eggs in hydrated stool pellets was enumerated in duplicate at the indicated time points for each mouse and displayed as egg number/stool weight. Mice were housed and handled following national guidelines and as approved by our Animal Review Committee.

SHIP1^−/− (CD45.1) mice have been previously described.(Wang et al., 2002 (link)) C57BL/6-CD45.2 (B6.2), C57BL/6-CD45.1 (B6.1) and BALB/c (H2^d) mice were purchased from Jackson Laboratories and Taconic, were at least 8 weeks old at the time of experimentation. All mice were housed at the Upstate Medical University Department of Laboratory Animal Resources Facility for at least one week prior to start of experimentations under standard husbandry conditions. All experiments were performed with the approval of the Institutional Animal Care and Use Committee.