InVivoPlus rat IgG2b isotype control, anti-keyhole limpet hemocyanin
Product Description
Specifications
| Isotype | Rat IgG2b, κ |
|---|---|
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin* |
≤0.5EU/mg (≤0.0005EU/μg) Determined by LAL assay |
| Aggregation* |
<5% Determined by SEC |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Purification | Protein G |
| RRID | AB_1107780 |
| Molecular Weight | 150 kDa |
| Murine Pathogen Tests* |
Ectromelia/Mousepox Virus: Negative Hantavirus: Negative K Virus: Negative Lactate Dehydrogenase-Elevating Virus: Negative Lymphocytic Choriomeningitis virus: Negative Mouse Adenovirus: Negative Mouse Cytomegalovirus: Negative Mouse Hepatitis Virus: Negative Mouse Minute Virus: Negative Mouse Norovirus: Negative Mouse Parvovirus: Negative Mouse Rotavirus: Negative Mycoplasma Pulmonis: Negative Pneumonia Virus of Mice: Negative Polyoma Virus: Negative Reovirus Screen: Negative Sendai Virus: Negative Theiler’s Murine Encephalomyelitis: Negative |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Application References
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Bauche, D., et al (2018). "LAG3(+) Regulatory T Cells Restrain Interleukin-23-Producing CX3CR1(+) Gut-Resident Macrophages during Group 3 Innate Lymphoid Cell-Driven Colitis" Immunity 49(2): 342-352 e345.
PubMed
Interleukin-22 (IL-22)-producing group 3 innate lymphoid cells (ILC3) maintains gut homeostasis but can also promote inflammatory bowel disease (IBD). The regulation of ILC3-dependent colitis remains to be elucidated. Here we show that Foxp3(+) regulatory T cells (Treg cells) prevented ILC3-mediated colitis in an IL-10-independent manner. Treg cells inhibited IL-23 and IL-1beta production from intestinal-resident CX3CR1(+) macrophages but not CD103(+) dendritic cells. Moreover, Treg cells restrained ILC3 production of IL-22 through suppression of CX3CR1(+) macrophage production of IL-23 and IL-1beta. This suppression was contact dependent and was mediated by latent activation gene-3 (LAG-3)-an immune checkpoint receptor-expressed on Treg cells. Engagement of LAG-3 on MHC class II drove profound immunosuppression of CX3CR1(+) tissue-resident macrophages. Our study reveals that the health of the intestinal mucosa is maintained by an axis driven by Treg cells communication with resident macrophages that withhold inflammatory stimuli required for ILC3 function.
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Triplett, T. A., et al (2018). "Reversal of indoleamine 2,3-dioxygenase-mediated cancer immune suppression by systemic kynurenine depletion with a therapeutic enzyme" Nat Biotechnol 36(8): 758-764.
PubMed
Increased tryptophan (Trp) catabolism in the tumor microenvironment (TME) can mediate immune suppression by upregulation of interferon (IFN)-gamma-inducible indoleamine 2,3-dioxygenase (IDO1) and/or ectopic expression of the predominantly liver-restricted enzyme tryptophan 2,3-dioxygenase (TDO). Whether these effects are due to Trp depletion in the TME or mediated by the accumulation of the IDO1 and/or TDO (hereafter referred to as IDO1/TDO) product kynurenine (Kyn) remains controversial. Here we show that administration of a pharmacologically optimized enzyme (PEGylated kynureninase; hereafter referred to as PEG-KYNase) that degrades Kyn into immunologically inert, nontoxic and readily cleared metabolites inhibits tumor growth. Enzyme treatment was associated with a marked increase in the tumor infiltration and proliferation of polyfunctional CD8(+) lymphocytes. We show that PEG-KYNase administration had substantial therapeutic effects when combined with approved checkpoint inhibitors or with a cancer vaccine for the treatment of large B16-F10 melanoma, 4T1 breast carcinoma or CT26 colon carcinoma tumors. PEG-KYNase mediated prolonged depletion of Kyn in the TME and reversed the modulatory effects of IDO1/TDO upregulation in the TME.
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Sledzinska, A., et al (2013). "TGF-beta signalling is required for CD4(+) T cell homeostasis but dispensable for regulatory T cell function" PLoS Biol 11(10): e1001674.
PubMed
TGF-beta is widely held to be critical for the maintenance and function of regulatory T (T(reg)) cells and thus peripheral tolerance. This is highlighted by constitutive ablation of TGF-beta receptor (TR) during thymic development in mice, which leads to a lethal autoimmune syndrome. Here we describe that TGF-beta-driven peripheral tolerance is not regulated by TGF-beta signalling on mature CD4(+) T cells. Inducible TR2 ablation specifically on CD4(+) T cells did not result in a lethal autoinflammation. Transfer of these TR2-deficient CD4(+) T cells to lymphopenic recipients resulted in colitis, but not overt autoimmunity. In contrast, thymic ablation of TR2 in combination with lymphopenia led to lethal multi-organ inflammation. Interestingly, deletion of TR2 on mature CD4(+) T cells does not result in the collapse of the T(reg) cell population as observed in constitutive models. Instead, a pronounced enlargement of both regulatory and effector memory T cell pools was observed. This expansion is cell-intrinsic and seems to be caused by increased T cell receptor sensitivity independently of common gamma chain-dependent cytokine signals. The expression of Foxp3 and other regulatory T cells markers was not dependent on TGF-beta signalling and the TR2-deficient T(reg) cells retained their suppressive function both in vitro and in vivo. In summary, absence of TGF-beta signalling on mature CD4(+) T cells is not responsible for breakdown of peripheral tolerance, but rather controls homeostasis of mature T cells in adult mice.
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Erickson, J. J., et al (2014). "Programmed death-1 impairs secondary effector lung CD8(+) T cells during respiratory virus reinfection" J Immunol 193(10): 5108-5117.
PubMed
Reinfections with respiratory viruses are common and cause significant clinical illness, yet precise mechanisms governing this susceptibility are ill defined. Lung Ag-specific CD8(+) T cells (T(CD8)) are impaired during acute viral lower respiratory infection by the inhibitory receptor programmed death-1 (PD-1). To determine whether PD-1 contributes to recurrent infection, we first established a model of reinfection by challenging B cell-deficient mice with human metapneumovirus (HMPV) several weeks after primary infection, and found that HMPV replicated to high titers in the lungs. A robust secondary effector lung TCD8 response was generated during reinfection, but these cells were more impaired and more highly expressed the inhibitory receptors PD-1, LAG-3, and 2B4 than primary T(CD8). In vitro blockade demonstrated that PD-1 was the dominant inhibitory receptor early after reinfection. In vivo therapeutic PD-1 blockade during HMPV reinfection restored lung T(CD8) effector functions (i.e., degranulation and cytokine production) and enhanced viral clearance. PD-1 also limited the protective efficacy of HMPV epitope-specific peptide vaccination and impaired lung T(CD8) during heterotypic influenza virus challenge infection. Our results indicate that PD-1 signaling may contribute to respiratory virus reinfection and evasion of vaccine-elicited immune responses. These results have important implications for the design of effective vaccines against respiratory viruses.
Product Citations
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Biomimetic vesicles engineered from modified tumour cells act as personalized vaccines for post-surgical cancer immunotherapy.
In Nat Nanotechnol on 1 March 2026 by Yu, P., Jin, Z., et al.
PubMed
Surgical resection remains the primary treatment for most solid tumours, yet metastatic tumour cells remaining after surgery substantially contribute to cancer-related mortality and recurrence. Here we identify syntaxin 11 as a key regulator that enhances the expression of MHC I and co-stimulatory molecules CD80/CD86 on tumour cell membranes, enabling cancer cells to acquire dendritic-cell-like features. By overexpressing syntaxin 11 in autologous tumour cells obtained from surgical resections, we generated MHC Ihigh/CD80high/CD86high dendritic-cell-like cells. Utilizing the cell membranes of these modified cells, we engineered artificial dendritic-cell-like cell-derived vesicles as a personalized autologous nanovaccine for the immunotherapy of postoperative metastatic cancer. This nanovaccine substantially improves antigen delivery to lymphoid organs and enhances antigen presentation efficiency through tumour self-presentation, thereby disrupting traditional vaccine development paradigms. Our work provides a promising avenue for developing effective metastatic cancer immunotherapies and offers hope for personalized postoperative immunotherapy.
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Targeting macrophages prevents alloantibody-mediated platelet clearance in a murine model of transfusion refractoriness.
In Blood Adv on 27 January 2026 by Rojas Jiménez, G., Angénieux, C., et al.
PubMed
HLA class I-immunized patients can experience a serious complication known as platelet transfusion refractoriness (PTR). This issue becomes especially relevant in onco-hematology departments where platelet transfusions are at the heart of patient care. Although transfusion failure is evidenced by a rapid elimination of allogeneic platelets from the recipient's bloodstream, the mechanisms behind it remain poorly characterized. The aim of this study was to better define these mechanisms to improve therapy for PTR. Using a murine model of major histocompatibility complex class I incompatibility to mimic PTR, we first established that antibodies, but not natural killer or CD8 cells, mediated platelet clearance. However, blocking Fcγ receptors with intravenous immunoglobulin or a monoclonal antibody or complement depletion did not correct refractoriness in alloimmune mice. Therefore, we investigated other alternatives beyond antibody-dependent mechanisms. Flow cytometric and microscopic analysis showed that Kupffer cells in the liver and red pulp macrophages in the spleen phagocytose allogeneic platelets during PTR. Moreover, intravital microscopy revealed allogeneic platelets retained in close interaction with macrophages in the red pulp only in alloimmune animals. Splenectomy or Kupffer cell depletion with clodronate in alloimmune mice suggested the existence of compensatory elimination mechanisms in the liver and spleen. Therefore, the simultaneous removal of both macrophage populations was an effective strategy to abrogate PTR. Our study provides an insight into the mechanisms of platelet clearance in alloimmune pathologies and opens up new perspectives for therapeutic targets.
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Intratumoral dendritic cell immunotherapy controls dissemination of metastasis-initiating cancer cells, even in patients with metastatic breast cancer.
In J Immunother Cancer on 6 January 2026 by Soyano, A., Lee, M. C., et al.
PubMed
Patients with metastatic breast cancer (MBC) have limited opportunities for a cure, as they develop resistance to therapies and continually form new metastases. Clinical overt metastases emerge from metastasis-initiating cancer cells (MICs) that disseminate during breast cancer (BC) progression. Currently, there are no available therapies that inhibit MIC dissemination to prevent overt metastasis. We provide preclinical evidence that intratumoral (IT) delivery of type I polarized dendritic cells (DC1) limited the MIC dissemination mechanisms in tumor lesions of human epidermal growth factor receptor 2 (HER2)+ mammary carcinoma. Interferon gamma, a prominent cytokine secreted by T helper 1 and innate-like immune effector cells, inhibited dissemination of MICs from the tumor lesions via the modulation of HER2/progesterone receptor/Wnt family member 4/receptor activator of nuclear factor kappa beta ligand signaling. Importantly, we provide clinical evidence that in patients with stage I-III HER2+ BC, there was significant regression of the primary tumor treated with IT DC1, as well as inhibition of disseminating MIC phenotypes. We observed a reduced burden of MICs in the bone marrow (BM) of patients with stage I-III HER2+BC treated with IT DC1, compared with untreated patients and those treated with standard neoadjuvant HER2 therapies paclitaxel, with or without carboplatin, trastuzumab and pertuzumab (Taxol, Carboplatin, Herceptin and Perjeta or THP). We also treated a single patient with de novo stage IV HER2+ MBC with trastuzumab, pertuzumab and tamoxifen in combination with IT DC1. Remarkably, this treatment resulted in near-complete regression of primary tumor and metastatic disease, along with inhibition of MIC seeding in the BM. These findings suggest an intriguing strategy to inhibit the dissemination of MICs and prevent further overt metastasis in all patients with BC.
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Smohaze-Upregulated RFWD3 Competes with TRIM24 to Stabilize TREX1 and Reduce Cytosolic dsDNA in Non-Small Cell Lung Cancer.
In Adv Sci (Weinh) on 1 December 2025 by Shi, X. Y., Shen, Y. K., et al.
PubMed
The three-prime repair exonuclease 1 (TREX1), an intracellular double-stranded DNA (dsDNA) degrader that inhibits the stimulator of interferon (IFN) genes (STING) pathway, is turned over by E3 ligase TRIM24-mediated proteasomal degradation. To uncover TREX1-stabilizers in non-small cell lung cancer (NSCLC), mass spectrometry is conducted, and 374 candidates are identified, with the RING Finger and WD Repeat Domain 3 (RFWD3) as a TREX1 protector that sequesters it from TRIM24. Overexpression of RFWD3 promotes tumor growth with increased myeloid-derived suppressor cells (MDSCs), while inhibition of RFWD3 increases intracellular dsDNA levels, activates the STING-IFN signaling, decreases MDSCs, and enhances the efficacy of PD-L1 blockade in murine NSCLC models. Furthermore, smoker patients have higher RFWD3 levels than non-smoker patients, and cigarette smoke extract, PM2.5, and benzo(a)pyrene upregulatesRFWD3 via transcription factor aryl hydrocarbon receptor. These results indicate a role of RFWD3 in tobacco smoke and haze (smohaze)-promoted immune evasion, inhibition of which activates STING-IFN signaling and synergizes with immune checkpoint inhibitors in NSCLC.