Advances in understanding immune response in dairy cattle

2021 ◽  
pp. 121-162
Author(s):  
Bonnie Mallard ◽  
◽  
Mehdi Emam ◽  
Shannon Cartwright ◽  
Tess Altvater-Hughes ◽  
...  
Keyword(s):  
Dairy Cattle ◽  
T Cell Receptor ◽  
Neutralizing Antibodies ◽  
Foot And Mouth Disease ◽  
Cell Receptor ◽  
Γδ T Cell ◽  
E Coli ◽  
Mouth Disease Virus ◽  
Complementarity Determining Region

From the beginning, cattle have made important contributions to the field of immunology, including the development of the first Mycobacterium bovis BCG vaccine for human tuberculosis in 1921. In 1981 the first report of a biosynthesized polypeptide vaccine against Foot and Mouth Disease Virus (FMDV) using the VP3 protein expressed in Escherichia coli (E. coli) was made for cattle. Cattle also possess a substantial proportion of T cells expressing the γδ T-cell receptor which helped to elucidate the role of these unique cells in host defence. More recently, it was discovered that cattle produce antibodies with ultra-long Complementarity Determining Region (CDR) - 3. This seminal finding has allowed the production of bovine therapeutic broadly neutralizing antibodies with ultra-long CDRs to passively treat various virial infections in humans and play a key role in protecting cattle. This chapter will review advances in bovine immunology, particularly as it relates to dairy cattle.

scholarly journals Immunosurveillance by human γδ T lymphocytes: the emerging role of butyrophilins

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 782 ◽  
Author(s):  
Dieter Kabelitz ◽  
Marcus Lettau ◽  
Ottmar Janssen
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
T Cell Receptor ◽  
T Cell Activation ◽  
Γδ T Cells ◽  
Cellular Transformation ◽  
Cell Receptor ◽  
Γδ T Cell

In contrast to conventional T lymphocytes, which carry an αβ T-cell receptor and recognize antigens as peptides presented by major histocompatibility complex class I or class II molecules, human γδ T cells recognize different metabolites such as non-peptidic pyrophosphate molecules that are secreted by microbes or overproduced by tumor cells. Hence, γδ T cells play a role in immunosurveillance of infection and cellular transformation. Until recently, it has been unknown how the γδ T-cell receptor senses such pyrophosphates in the absence of known antigen-presenting molecules. Recent studies from several groups have identified a unique role of butyrophilin (BTN) protein family members in this process, notably of BTN3A1. BTNs are a large family of transmembrane proteins with diverse functions in lipid secretion and innate and adaptive immunity. Here we discuss current models of how BTN molecules regulate γδ T-cell activation. We also address the implications of these recent findings on the design of novel immunotherapeutic strategies based on the activation of γδ T cells.

scholarly journals Essential and Partially Overlapping Role of CD3γ and CD3δ for Development of αβ and γδ T Lymphocytes

1998 ◽  
Vol 188 (7) ◽  
pp. 1375-1380 ◽  
Author(s):  
Baoping Wang ◽  
Ninghai Wang ◽  
Mariolina Salio ◽  
Arlene Sharpe ◽  
Deborah Allen ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Gene Knockout ◽  
Γδ T Cells ◽  
Cell Receptor ◽  
Γδ T Cell ◽  
Thymic Development ◽  
Gene Knockout Mice

CD3γ and CD3δ are two highly related components of the T cell receptor (TCR)–CD3 complex which is essential for the assembly and signal transduction of the T cell receptor on mature T cells. In gene knockout mice deficient in either CD3δ or CD3γ, early thymic development mediated by pre-TCR was either undisturbed or severely blocked, respectively, and small numbers of TCR-αβ+ T cells were detected in the periphery of both mice. γδ T cell development was either normal in CD3δ−/− mice or partially blocked in CD3γ−/− mice. To examine the collective role of CD3γ and CD3δ in the assembly and function of pre-TCR and in the development of γδ T cells, we generated a mouse strain with a disruption in both CD3γ and CD3δ genes (CD3γδ−/−). In contrast to mice deficient in either CD3γ or CD3δ chains, early thymic development mediated by pre-TCR is completely blocked, and TCR-αβ+ or TCR-γδ+ T cells were absent in the CD3γδ−/− mice. Taken together, these studies demonstrated that CD3γ and CD3δ play an essential, yet partially overlapping, role in the development of both αβ and γδ T cell lineages.

scholarly journals The TCR ligand-inducible expression of CD73 marks γδ lineage commitment and a metastable intermediate in effector specification

2014 ◽  
Vol 211 (2) ◽  
pp. 329-343 ◽  
Author(s):  
Francis Coffey ◽  
Sang-Yun Lee ◽  
Terkild B. Buus ◽  
Jens-Peter Holst Lauritsen ◽  
Gladys W. Wong ◽  
...  
Keyword(s):  
T Cell Receptor ◽  
Surface Protein ◽  
Intermediate Stage ◽  
Cell Receptor ◽  
Lineage Commitment ◽  
Cell Surface Protein ◽  
Γδ T Cell ◽  
Common Occurrence ◽  
Γδ T Cell Receptor

Numerous studies indicate that γδ T cell receptor (γδTCR) expression alone does not reliably mark commitment of early thymic progenitors to the γδ fate. This raises the possibility that the γδTCR is unable to intrinsically specify fate and instead requires additional environmental factors, including TCR–ligand engagement. We use single cell progenitor assays to reveal that ligand acts instructionally to direct adoption of the γδ fate. Moreover, we identify CD73 as a TCR ligand-induced cell surface protein that distinguishes γδTCR-expressing CD4−CD8− progenitors that have committed to the γδ fate from those that have not yet done so. Indeed, unlike CD73− γδTCR+ progenitors, which largely adopt the αβ fate upon separation from the intrathymic selecting environment, those that express CD73 remain CD4−CD8− and committed to the γδ fate. CD73 is expressed by >90% of peripheral γδ cells, suggesting this is a common occurrence during development. Moreover, CD73 induction appears to mark a metastable intermediate stage before acquisition of effector function, suggesting that γδ lineage and effector fate are specified sequentially. These findings have important implications for the role of ligand in γδ lineage commitment and its relationship to the specification of effector fate.

scholarly journals The T Cell Receptor (TRB) Locus in Tursiops truncatus: From Sequence to Structure of the Alpha/Beta Heterodimer in the Human/Dolphin Comparison

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 571
Author(s):  
Giovanna Linguiti ◽  
Sofia Kossida ◽  
Ciro Leonardo Pierri ◽  
Joumana Jabado-Michaloud ◽  
Geraldine Folch ◽  
...  
Keyword(s):  
Amino Acids ◽  
T Cell ◽  
T Cell Receptor ◽  
Tursiops Truncatus ◽  
Cell Receptor ◽  
Sequence Alignments ◽  
T Cell Receptor Beta ◽  
Alpha Beta ◽  
Receptor Beta ◽  
Complementarity Determining Region

The bottlenose dolphin (Tursiops truncatus) belongs to the Cetartiodactyla and, similarly to other cetaceans, represents the most successful mammalian colonization of the aquatic environment. Here we report a genomic, evolutionary, and expression study of T. truncatus T cell receptor beta (TRB) genes. Although the organization of the dolphin TRB locus is similar to that of the other artiodactyl species, with three in tandem D-J-C clusters located at its 3′ end, its uniqueness is given by the reduction of the total length due essentially to the absence of duplications and to the deletions that have drastically reduced the number of the germline TRBV genes. We have analyzed the relevant mature transcripts from two subjects. The simultaneous availability of rearranged T cell receptor α (TRA) and TRB cDNA from the peripheral blood of one of the two specimens, and the human/dolphin amino acids multi-sequence alignments, allowed us to calculate the most likely interactions at the protein interface between the alpha/beta heterodimer in complex with major histocompatibility class I (MH1) protein. Interacting amino acids located in the complementarity-determining region according to IMGT numbering (CDR-IMGT) of the dolphin variable V-alpha and beta domains were identified. According to comparative modelization, the atom pair contact sites analysis between the human MH1 grove (G) domains and the T cell receptor (TR) V domains confirms conservation of the structure of the dolphin TR/pMH.

scholarly journals Ceramide Synthase 2 Null Mice Are Protected from Ovalbumin-Induced Asthma with Higher T Cell Receptor Signal Strength in CD4+ T Cells

2021 ◽  
Vol 22 (5) ◽  
pp. 2713
Author(s):  
Sun-Hye Shin ◽  
Kyung-Ah Cho ◽  
Hee-Soo Yoon ◽  
So-Yeon Kim ◽  
Hee-Yeon Kim ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cd4 T Cells ◽  
Acyl Chain ◽  
Signal Strength ◽  
Cell Receptor ◽  
Ceramide Synthase ◽  
Asthmatic Patients

(1) Background: six mammalian ceramide synthases (CerS1–6) determine the acyl chain length of sphingolipids (SLs). Although ceramide levels are increased in murine allergic asthma models and in asthmatic patients, the precise role of SLs with specific chain lengths is still unclear. The role of CerS2, which mainly synthesizes C22–C24 ceramides, was investigated in immune responses elicited by airway inflammation using CerS2 null mice. (2) Methods: asthma was induced in wild type (WT) and CerS2 null mice with ovalbumin (OVA), and inflammatory cytokines and CD4 (cluster of differentiation 4)+ T helper (Th) cell profiles were analyzed. We also compared the functional capacity of CD4+ T cells isolated from WT and CerS2 null mice. (3) Results: CerS2 null mice exhibited milder symptoms and lower Th2 responses than WT mice after OVA exposure. CerS2 null CD4+ T cells showed impaired Th2 and increased Th17 responses with concomitant higher T cell receptor (TCR) signal strength after TCR stimulation. Notably, increased Th17 responses of CerS2 null CD4+ T cells appeared only in TCR-mediated, but not in TCR-independent, treatment. (4) Conclusions: altered Th2/Th17 immune response with higher TCR signal strength was observed in CerS2 null CD4+ T cells upon TCR stimulation. CerS2 and very-long chain SLs may be therapeutic targets for Th2-related diseases such as asthma.

scholarly journals Foot-and-Mouth Disease Virus Viroporin 2B Antagonizes RIG-I-Mediated Antiviral Effects by Inhibition of Its Protein Expression

2016 ◽  
Vol 90 (24) ◽  
pp. 11106-11121 ◽  
Author(s):  
Zixiang Zhu ◽  
Guoqing Wang ◽  
Fan Yang ◽  
Weijun Cao ◽  
Ruoqing Mao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Foot And Mouth Disease ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Eukaryotic Translation ◽  
Mouth Disease Virus ◽  
2B Protein ◽  
Eukaryotic Translation Initiation ◽  
Cellular Apoptosis

ABSTRACTThe role of retinoic acid-inducible gene I (RIG-I) in foot-and-mouth disease virus (FMDV)-infected cells remains unknown. Here, we showed that RIG-I inhibits FMDV replication in host cells. FMDV infection increased the transcription of RIG-I, while it decreased RIG-I protein expression. A detailed analysis revealed that FMDV leader proteinase (Lpro), as well as 3C proteinase (3Cpro) and 2B protein, decreased RIG-I protein expression. Lproand 3Cproare viral proteinases that can cleave various host proteins and are responsible for several of the viral polyprotein cleavages. However, for the first time, we observed 2B-induced reduction of host protein. Further studies showed that 2B-mediated reduction of RIG-I is specific to FMDV, but not other picornaviruses, including encephalomyocarditis virus, enterovirus 71, and coxsackievirus A16. Moreover, we found the decreased protein level of RIG-I is independent of the cleavage of eukaryotic translation initiation factor 4 gamma, the induction of cellular apoptosis, or the association of proteasome, lysosome, and caspase pathways. A direct interaction was observed between RIG-I and 2B. The carboxyl-terminal amino acids 105 to 114 and amino acids 135 to 144 of 2B were essential for the reduction of RIG-I, while residues 105 to 114 were required for the interaction. These data suggest the antiviral role of RIG-I against FMDV and a novel antagonistic mechanism of FMDV that is mediated by 2B protein.IMPORTANCEThis study demonstrated that RIG-I could suppress FMDV replication during virus infection. FMDV infection increased the transcriptional expression of RIG-I, while it decreased RIG-I protein expression. FMDV 2B protein interacted with RIG-I and induced reduction of RIG-I. 2B-induced reduction of RIG-I was independent of the induction of the cleavage of eukaryotic translation initiation factor 4 gamma or cellular apoptosis. In addition, proteasome, lysosome, and caspase pathways were not involved in this process. This study provides new insight into the immune evasion mediated by FMDV and identifies 2B as an antagonistic factor for FMDV to evade the antiviral response.

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