Anti cd4 gk1

To deplete T cells, mice were intraperitoneally (i.p.) injected with 400ug anti-CD4 GK1.5 or anti-CD8 2.43 (BioXcell) in PBS at D-1, D4, and D10 relative to infection. To block T cell egress, mice were i.p. injected with 1mg/kg FTY720 (Sigma) in water daily starting 2d prior to harvest.

Pdcd1^−/− (Keir et al., 2007 (link)), LCMV GP33-specific TCR transgenic “P14”, Pdcd1^+/+ P14 (Odorizzi et al., 2015 (link)) and C57BL/6 mice (Charles River) were housed at the University of Pennsylvania (Philadelphia, PA) and treated in accordance with protocols approved by the Institutional Animal Care and Use Committee. Infections with LCMV Armstrong (2 × 10⁵ plaque-forming units (PFU) i.p.) or clone 13 (4 × 10⁶ PFU i.v.) were performed as described (Odorizzi et al., 2015 (link)). Treatment with 300µg/kg of rapamycin or PBS was performed daily at d5–8 p.i. For antibody blockade, mice were injected with 200µg anti-CD4 (GK1.5; BioXcell) i.p. on day −1 and +1 of infection; treatment with 200µg anti-PDL1 (10F.9G2) antibody or isotype control was performed every three days between d22–35 p.i. For cotransfer experiments, 250 Pdcd1^+/+ and Pdcd1^−/− P14 cells were adoptively transferred as described (Odorizzi et al., 2015 (link)).

Unless otherwise specified, all mouse infections with Lm, Yp and Cr were performed with foodborne infection as previously described.^{11 (link), 13 (link)} Bacterial strains and infection doses are summarized in Table S3. GF and SPF control mice were infected by oral gavage with 1×10⁸ CFU InlA^MLm, strain 10403s due to the increased susceptibility of GF mice to foodborne Lm infection. For STm infections, naïve mice were left untreated or orally treated with 20 mg streptomycin solution in PBS one day prior to intragastric inoculation of STm. Systemic infection with Cr was performed through a single i.p. injection. When indicated, mice were given i.p. injections of 100 μg anti-Cδ TCR (GL4 or UC7–13D5, Bio X Cell), 200 μg anti-CD4 (GK1.5, Bio X Cell) or 500 μg anti-CD8α (2.43, Bio X Cell) antibody, alone or in combination, or PBS on days −3, −1 and +1 relative to recall infection.

The bilateral subcutaneous model was established as for the in vivo anti-cancer efficacy. When the primary tumors reached 100–150 mm³ in volume, mice were injected intratumorally with nMOFs at a dose of 0.11 mg/mouse or PBS. Anti-CD4 (GK1.5, BioXCell, USA), anti-CD8 (OKT-8, BioXCell, USA), mouse IgG (C1.18.4, BioXCell, USA) antibodies Or B cell inhibitor ibrutinib (PCI-32765, Selleckchem) were intraperitoneally injected into the mice (200 μg/mouse) on Day 0 and 5 after the first treatment. Twelve hours post-injection, mice were anesthetized with 2% (v/v) isoflurane, and tumors were irradiated with X-ray at 225 kVp and 13 mA with a 0.3-mm Cu filter. To evaluate the therapeutic efficacy, the tumor growth and body weight were monitored daily.

Mice were intraperitoneally (i.p.) injected with 200µg anti-CD8a (53-6.72, BioXcell), anti-CD4 (GK1.5, BioXcell), anti-NK1.1 (PK-136, BioXcell), anti-TNFα (XT3.11, BioXcell), anti-IFN (XMG1.2, BioXcell), anti-IL-17a (17F3, BioXcell) antibodies or IgG one day before tumor cell injection, and further the treatment was continued on days 2, 5, and 8 with 150µg antibodies. 1µg recombinant murine TNF (Peprotech) or vehicle were i.p. injected as above.