Molecular characterization and expression analysis of interferon γ (IFN-γ) gene in Labeo rohita (Ham.)

Parhi, Janmejay; Sahoo, Lakshman; Choudhury, Jyotibrata; Choudhury, Tanmoy Gon; Baruah, Arunjyoti; Paniprasad, K.; Makesh, M.

doi:10.1016/j.aqrep.2015.08.007

Cited by 12 publications

(2 citation statements)

References 26 publications

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“…In another study microarray analysis gave similar equivocal ifnγ change in kidney tissue of Rag1 -/- zebrafish [ 9 ]. Others documented induction of kidney ifnγ expression following Poly I:C treatment in Atlantic salmon [ 67 ], rainbow trout [ 42 ], grass carp [ 59 ], Labeo rohita [ 73 ], and WT zebrafish [ 66 ]. Poly I:C treatment had no effect on ifnγ expression in mutant zebrafish spleens.…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression following TLR stimulation in rag1-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations

et al. 2017

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In the absence of lymphocytes, rag1-/- mutant zebrafish develop protective immunity to bacteria. In mammals, induction of protection by innate immunity can be mediated by macrophages or natural killer (NK) cells. To elucidate potential responsive cell populations, we morphologically characterized lymphocyte-like cells (LLCs) from liver, spleen and kidney hematopoietic tissues. In fish, these cells include NK cells and Non-specific cytotoxic cells (NCCs). We also evaluated the transcriptional expression response of select genes that are important indicators of NK and macrophage activation after exposure to specific TLR ligands. The LLC cell populations could be discriminated by size and further discriminated by the presence of cytoplasmic granules. Expression levels of mx, tnfα, ifnγ, t-bet and nitr9 demonstrated dynamic changes in response to intra-coelomically administered β glucan (a TLR2/6 ligand), Poly I:C (a TLR3 ligand) and resiquimod (R848) (a TLR7/8 ligand). Following TLR 2/6 stimulation, there was a greater than 100 fold increase in ifnγ in liver, kidney and spleen and moderate increases in tnfα in liver and kidney. TLR3 stimulation caused broad up regulation of mx, down-regulation of tnfα in kidney and spleen tissues and up regulation of nitr9 in the kidney. Following TLR 7/8 stimulation, there was a greater than 100 fold increase in ifnγ in liver and kidney and t-bet in liver. Our gene expression findings suggest that LLCs and macrophages are stimulated following β glucan exposure. Poly I:C causes type I interferon response and mild induction of LLC in the kidney and R-848 exposure causes the strongest LLC stimulation. Overall, the strongest NK like gene expression occurred in the liver. These differential effects of TLR ligands in rag1-/- mutant zebrafish shows strong NK cell-like gene expression responses, especially in the liver, and provides tools to evaluate the basis for protective immunity mediated by the innate immune cells of fish.

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Section: Discussionmentioning

confidence: 99%

Differential gene expression following TLR stimulation in rag1-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations

et al. 2017

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“…Interferon gamma (IFNγ) is a soluble pleiotropic cytokine member of type II class of interferons ( 1 ). This molecule has been described in many groups of vertebrates, such as chondrichthyes, jawed fish, amphibians, birds and mammals, suggesting that IFNγ appeared at least 450 million years ago, before the divergence between fish and tetrapods ( 2 ).…”

Section: Introductionmentioning

confidence: 99%

Interferon Gamma Induces the Increase of Cell-Surface Markers (CD80/86, CD83 and MHC-II) in Splenocytes From Atlantic Salmon

et al. 2021

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Type II interferon gamma (IFNγ) is a pleiotropic cytokine capable of modulating the innate and adaptive immune responses which has been widely characterized in several teleost families. In fish, IFNγ stimulates the expression of cytokines and chemokines associated with the pro-inflammatory response and enhances the production of nitrogen and oxygen reactive species in phagocytic cells. This work studied the effect of IFNγ on the expression of cell-surface markers on splenocytes of Atlantic salmon (Salmo salar). In vitro results showed that subpopulations of mononuclear splenocytes cultured for 15 days were capable of increasing gene expression and protein availability of cell-surface markers such as CD80/86, CD83 and MHC II, after being stimulated with recombinant IFNγ. These results were observed for subpopulations with characteristics associated with monocytes (51%), and features that could be related to lymphocytes (46.3%). In addition, a decrease in the expression of zbtb46 was detected in IFNγ-stimulated splenocytes. Finally, the expression of IFNγ and cell-surface markers was assessed in Atlantic salmon under field conditions. In vivo results showed that the expression of ifnγ increased simultaneously with the up-regulation of cd80/86, cd83 and mhcii during a natural outbreak of Piscirickettsia salmonis. Overall, the results obtained in this study allow us to propose IFNγ as a candidate molecule to stimulate the phenotypic progression of a small population of immune cells, which will increase antigen presenting cells markers. Thereby, modulatory strategies using IFNγ may generate a robust and coordinated immune response in fish against pathogens that affect aquaculture.

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Overview of Fish Immune System

Makesh¹,

Bedekar²,

Rajendran³

2022

Fish Immune System and Vaccines

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Molecular characterization and expression analysis of interferon γ (IFN-γ) gene in Labeo rohita (Ham.)

Cited by 12 publications

References 26 publications

Differential gene expression following TLR stimulation in rag1-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations

Differential gene expression following TLR stimulation in rag1-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations

Interferon Gamma Induces the Increase of Cell-Surface Markers (CD80/86, CD83 and MHC-II) in Splenocytes From Atlantic Salmon

Overview of Fish Immune System

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