The bovine leukemia virus infection prolongs immunosuppression in dairy cows during the periparturient period by sustaining higher expression of immunological checkpoints in T cells

IF 1.4 3区 农林科学 Q4 IMMUNOLOGY
Alice Maria Melo do Nascimento , Carolina Menezes Suassuna de Souza , Ana Claudia Dumont Oliveira , Maiara Garcia Blagitz , Eduardo Milton Ramos Sanchez , Alice Maria Melville Paiva Della Libera , Ricardo de Miranda Henriques Leite , Artur Cezar de Carvalho Fernandes , Fernando Nogueira Souza
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引用次数: 0

Abstract

Bovine leukemia virus (BLV) is caused by a deltaretrovirus and has been associated with immunosuppression as well as comorbidities such as bovine mastitis, the costliest disease in the dairy sector. However, no previous study has explored at the synergistic immunosuppressive effect of the peripartum period with an immunosuppressive viral disease such as BLV. Thus, our study explored the effect of BLV infection in the periparturient period on the expression of PD-1 and CTLA-4 in blood T lymphocytes, and the impact of BLV infection on the rate of new intramammary infections during the early lactation. Here, we found that BLV-infected dairy cows always had a statistically significant higher expression of CTLA-4 and PD-1 in blood T cells. Furthermore, our findings indicated that BLV infection prolongs immunosuppression in dairy cows during the periparturient period by sustaining higher expression of immunological checkpoints in T cells. In addition, BLV-infected dairy cows have a higher rate of new intramammary infections during early lactation. Thus, our study provides new insights of the immunosuppressive effect of BLV on the most critical period of the cows’ life with marked detrimental effect on protective T-cell immunity and comorbidities, such as bovine mastitis.

牛白血病病毒感染通过维持T细胞免疫检查点的高表达,延长奶牛围产期的免疫抑制
牛白血病病毒(BLV)由三角逆转录病毒引起,并与免疫抑制以及合并症(如奶牛乳腺炎)有关,乳腺炎是乳制品行业最昂贵的疾病。然而,目前尚无研究探讨围产期与BLV等免疫抑制性病毒疾病的协同免疫抑制作用。因此,本研究探讨围产期BLV感染对外周血T淋巴细胞PD-1和CTLA-4表达的影响,以及BLV感染对泌乳早期乳腺内新发感染率的影响。在这里,我们发现blv感染奶牛的血液T细胞中CTLA-4和PD-1的表达始终具有统计学意义。此外,我们的研究结果表明,BLV感染通过维持T细胞免疫检查点的高表达,延长了奶牛在围产卵期的免疫抑制。此外,blv感染的奶牛在泌乳早期有较高的新乳内感染率。因此,我们的研究为BLV在奶牛生命的最关键时期的免疫抑制作用提供了新的见解,并对保护性t细胞免疫和牛乳腺炎等合并症产生了明显的不利影响。
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来源期刊
CiteScore
3.40
自引率
5.60%
发文量
79
审稿时长
70 days
期刊介绍: The journal reports basic, comparative and clinical immunology as they pertain to the animal species designated here: livestock, poultry, and fish species that are major food animals and companion animals such as cats, dogs, horses and camels, and wildlife species that act as reservoirs for food, companion or human infectious diseases, or as models for human disease. Rodent models of infectious diseases that are of importance in the animal species indicated above,when the disease requires a level of containment that is not readily available for larger animal experimentation (ABSL3), will be considered. Papers on rabbits, lizards, guinea pigs, badgers, armadillos, elephants, antelope, and buffalo will be reviewed if the research advances our fundamental understanding of immunology, or if they act as a reservoir of infectious disease for the primary animal species designated above, or for humans. Manuscripts employing other species will be reviewed if justified as fitting into the categories above. The following topics are appropriate: biology of cells and mechanisms of the immune system, immunochemistry, immunodeficiencies, immunodiagnosis, immunogenetics, immunopathology, immunology of infectious disease and tumors, immunoprophylaxis including vaccine development and delivery, immunological aspects of pregnancy including passive immunity, autoimmuity, neuroimmunology, and transplanatation immunology. Manuscripts that describe new genes and development of tools such as monoclonal antibodies are also of interest when part of a larger biological study. Studies employing extracts or constituents (plant extracts, feed additives or microbiome) must be sufficiently defined to be reproduced in other laboratories and also provide evidence for possible mechanisms and not simply show an effect on the immune system.
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