文献

重组大鼠IgG2a同型对照抗体，体内实验级（In Vivo Grade Recombinant Rat IgG2a Isotype Control Antibody，Syd Labs PA007143）

大鼠IgG抗体主要依据重链的同型分为四个亚类（重链包括IgG1、IgG2a、IgG2b和IgG2c；轻链包括κ型和λ型），其中IgG1与κ型是血清中含量最高的类型。IgG抗体是分子量约150 kDa的大分子，由四条肽链组成：两条相同的重链，分子量约50 kDa；两条相同的轻链，分子量约25 kDa。依靠两条重链之间、重链与轻链之间形成的二硫键，四条肽链组装成Y型四聚体。

大鼠IgG2a同型对照及其突变体（天然及工程改造型rtIgG2a同型对照）可用于多种体外、体内研究中的动物模型功能学实验，适用实验包含ELISA、蛋白免疫印迹（WB）、流式细胞术（Flow）、免疫沉淀（IP）、石蜡切片免疫组化（IHC(P)）以及冰冻切片免疫组化（IHC(F)）。相较于大鼠IgG2b抗体，大鼠IgG2a、IgG1抗体特性更接近小鼠IgG1抗体。大部分大鼠来源抗体被用于研究小鼠及人源靶蛋白。

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大鼠IgG2a同型对照抗体部分参考文献：

1.TIGIT predominantly regulates the immune response via regulatory T cells.
Kurtulus, S., et al. J Clin Invest. 2015 Nov;125(11):4053-62. PMID: 26413872
“In some experiments, mice were treated with 250 μg isotype (rat IgG2a) or anti–TIM-3 Abs on the days indicated in the legend for Figure 7. …A recent study suggests that TIGIT regulates T cell function by inhibiting CD226 dimerization and downstream signaling. …Upregulation of these receptors on effector T cells terminates T cell responses, while their expression on Tregs promotes their suppressor function. …T cell Ig and ITIM domain (TIGIT) is a recently identified coinhibitory receptor that is found on the surface of a variety of lymphoid cells, and its role in immune regulation is just beginning to be elucidated. …We demonstrated that TIGIT signaling in Tregs directs their phenotype and that TIGIT primarily suppresses antitumor immunity via Tregs and not CD8+ T cells. Moreover, TIGIT+ Tregs upregulated expression of the coinhibitory receptor TIM-3 in tumor tissue, and TIM-3 and TIGIT synergized to suppress antitumor immune responses.”

2.Animal model of respiratory syncytial virus: CD8+ T cells cause a cytokine storm that is chemically tractable by sphingosine-1-phosphate 1 receptor agonist therapy.
Walsh, K. B., et al. J Virol. 2014 Jun;88(11):6281-93. PMID: 24672024
“For cell depletion experiments, 250 μg of anti-NK1.1 and/or 500 μg of anti-CD8 antibodies were administered i.p. to mice 1 day before and 1 day after infection. Rat IgG2a was administered at equivalent concentrations for isotype control-treated mice within the cell depletion experiments. …The cytokine storm is an intensified, dysregulated, tissue-injurious inflammatory response driven by cytokine and immune cell components. …Now we describe a novel event where virus-specific T cells induce a cytokine storm. …The paramyxovirus pneumonia virus of mice (PVM) is a model of human respiratory syncytial virus (hRSV). …Blockading these cytokines with neutralizing antibodies blunts the cytokine storm and protects the host.”

3.The oestrous cycle stage affects mammary tumour sensitivity to chemotherapy.
Bornes, L., et al. Nature. 2025 Jan;637(8044):195-204. PMID: 39633046
“Individual mice were treated every week with either 60 mg kg−1 of either InVivoMAb anti-mouse CSF1R (CD115) monoclonal antibody or InVivoMAb rat IgG2a isotype control (BioXCell, clone 2A3, catalogue no. BE0089), or received InVivoMAb anti-mouse CD4 and InVivoMAb anti-mouse CD8 three times per week, every other day, with a first dose of 400 µg followed by 200 µg per antibody. …The response of breast cancer to neoadjuvant chemotherapy (NAC) varies substantially, even when tumours belong to the same molecular or histological subtype. …In three mouse models of breast cancer, we show reduced responses to NAC when treatment is initiated during the dioestrus stage, when compared with initiation during the oestrus stage. …Similar findings were observed in retrospective premenopausal cohorts of human patients. …Whereas NAC disrupts the oestrous cycle, this elevated macrophage prevalence persists and depletion of macrophages mitigates the reduced therapy response observed when initiating treatment during dioestrus.”

4.Chimeric antigen receptor macrophages (CAR-M) sensitize HER2+ solid tumors to PD1 blockade in pre-clinical models.
Pierini, S., et al. Nat Commun. 2025 Jan 15;16(1):706. PMID: 39814734
“In designated experiments, 10 µg/mL of InVivoMAb anti-mouse PD-1 or 10 µg/mL InVivoMAb rat IgG2a isotype control (BE0089, Bio X Cell) was added to the wells. …We previously developed human CAR macrophages (CAR-M) and demonstrated redirection of macrophage anti-tumor function leading to tumor control in immunodeficient xenograft models. …In vivo, anti-HER2 CAR-M significantly reduce tumor burden, prolong survival, remodel the TME, increase intratumoral T cell and natural killer (NK) cell infiltration, and induce antigen spreading. …CAR-M therapy protects against antigen-negative relapses in a T cell dependent fashion, confirming long-term anti-tumor immunity. …These results demonstrate synergy between CAR-M and T cell checkpoint blockade and provide a strategy to potentially enhance response to aPD1 therapy for patients with non-responsive tumors.”

5.Tamm-Horsfall protein augments neutrophil NETosis during urinary tract infection.
Mercado-Evans, V., et al. JCI Insight. 2025 Jan 9;10(1):e180024. PMID: 39589812
“Serial dilutions of homogenates and urine were plated on LB agar to enumerate CFU. For neutrophil depletion, mice injected i.p. with 10 μg of anti-Ly6G or rat IgG2a isotype in 100 μL prior to infection. …Urinary neutrophils are a hallmark of urinary tract infection (UTI), yet the mechanisms governing their activation, function, and efficacy in controlling infection remain incompletely understood. …Tamm-Horsfall glycoprotein (THP), the most abundant protein in urine, uses terminal sialic acids to bind an inhibitory receptor and dampen neutrophil inflammatory responses. …In a UTI model, THP-deficient mice showed elevated urinary tract bacterial burdens, increased neutrophil recruitment, and more severe tissue histopathological changes compared with WT mice. …These effects were observed only in the presence of a NETosis stimulus and could not be solely replicated with equivalent levels of sialic acid alone.”