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Written | The initiation of Qi immune response and the accumulation of lymphocytes in tissues both occur in the absence of inflammation, which is called steady-state immunity
.
It has been reported that the microbiota exposed on the skin surface can promote the accumulation of various lymphocyte subpopulations in the skin, thereby promoting tissue repair [1]
.
However, it is not clear how the immune system actively recognizes and responds to the microbiota in the absence of typical inflammatory processes
.
Interestingly, the microbiota can promote IFN-I production and antiviral status in tissues.
These findings seem to suggest that the microbiota can protect the host from viral infections [2]
.
Retroviruses can integrate as part of the host genome
.
Therefore, the long-term symbiotic relationship between mammals and microorganisms includes not only exogenous microorganisms (such as bacteria, fungi, and viruses), but also symbiotic relationships with endogenous retroviruses (ERVs) [3]
.
Most ERVs are in an inactive state; however, there are several ERVs expressing complete open reading frames, and their transcriptional activity is related to various physiological and pathological processes, so they are under constant immune pressure
.
Previous reports suggested that in some cases, microbial exposure can control the expression of ERVs [4], however, whether ERVs are directly involved in inducing responses to the microbiota is still unknown
.
In addition, under certain circumstances, the extent to which the high expression of ERVs may cause the inflammatory effects of the microbiota has not been resolved
.
On June 23, 2021, the Yasmine Belkaid team from the National Institutes of Health published an article entitled Endogenous retroviruses promote homeostatic and inflammatory responses to the microbiota in Cell.
In this study, the author proposed skin microbes Population can promote the expression of ERVs, and the intrinsic response of keratinocytes to ERVs depends on cGAS/STING signal transduction, and at the same time promotes the induction of T cells
.
If the reverse transcription of ERVs is inhibited, the microbial immune response and related tissue repair function will be impaired, and the high-fat diet can increase the expression of ERVs, which in turn leads to increased immune response and tissue inflammation
.
In summary, studies have shown that the host immune system uses the endogenous virus group to interact with the exogenous microbiota to regulate tissue repair or inflammation
.
The skin colonization of symbiotic bacteria often promotes the accumulation of various T cell subgroups in the skin in a way that is not coupled with the inflammatory process
.
For example, in the absence of tissue inflammation, mice with Staphylococcus epidermidis colonized on the skin surface are significantly up-regulated compared to SFP mice, many genes related to immune activation, among which are related to IFN-I and antiviral response The up-regulation of genes is the most obvious
.
It should be noted that previous reports pointed out that the induction of ERVs is related to the induction of IFN-I response, and the presence of Staphylococcus epidermidis is promoting the expression of several endogenous reverse transcription factor families
.
Next, the authors used mice treated with a combination of reverse transcriptase inhibitors to evaluate whether the cDNA synthesis of endogenous reverse transcriptase elements controls the T cell response to Staphylococcus epidermidis
.
Skin imaging shows that antiretroviral treatment can significantly inhibit the accumulation of T cells in the epidermis, and it can also significantly reduce the expression of IL-17 in CD8+, MAIT and γδ T cells in the skin
.
At the same time, scRNA-seq showed that this treatment also affected gene expression programs related to antibacterial defense and tissue repair
.
So what are the DNA sensors that may be involved in these reactions? Previous evidence has shown that retroviruses can activate cGAS to produce cGAMP, which further activates STING
.
Based on this, the authors verified that the absence of STING in keratinocytes can significantly reduce the number of all T cell subsets and the production of related cytokines
.
Although homeostasis of the microbiota promotes immune adaptability, conversely, the disorders of these symbiotic bacteria can also promote tissue inflammation
.
To test the possibility that ERVs may cause pathogenic effects on the microbiota, the authors used an intervention model that uses a high-fat diet to promote inflammation
.
Interestingly, there was no inflammation in the epidermis of mice on a normal diet, while epidermal hyperplasia and hyperkeratinization were significantly increased in mice on a high-fat diet.
At the same time, it was accompanied by high expression of inflammation-related genes and a variety of ERVs families
.
However, cGas-/-, Sting-/-, Ifnar1-/- mice have significantly reduced skin inflammation and epidermal hyperplasia under high-fat diet, confirming that the cGAS/STING/IFN-I axis is involved in the metabolism of the microbiota The ability to promote inflammation under changing circumstances
.
These findings are not only applicable to mouse models.
In order to evaluate this potential correlation with human skin inflammation, the authors also analyzed skin samples from psoriasis patients in this study.
The results showed that reverse transcription in psoriasis skin lesions The enzyme locus is strongly induced relative to normal skin, which means that skin inflammation in mice and humans may be related to the enhanced expression of ERVs
.
In general, this study puts forward the view that the host may choose the endogenous virus group as a means of communicating with the exogenous microbiota, and the immune response to the microbiota under steady-state immunity and inflammation.
The degree of ERVs is controlled by the expression of ERVs.
Therefore, the response of ERVs to microorganisms should be integrated into our understanding of diseases and inflammatory states
.
Original link: https://doi.
org/10.
1016/j.
cell.
2021.
05.
020 Platemaker: 11 References 1.
Belkaid, Y.
, and Harrison, OJ (2017).
Homeostatic immunity and the microbiota.
Immunity 46 , 562–576.
2.
Abt, MC, Osborne, LC, Monticelli, LA, Doering, TA, Alenghat, T.
, Sonnenberg, GF, Paley, MA, Antenus, M.
, Williams, KL, Erikson, J.
, et al .
(2012).
Commensal bacteria calibrate the activation threshold of innate antiviral immunity.
Immunity 37, 158–170.
3.
Johnson, WE (2015).
Endogenous retroviruses in the genomics era.
Annu.
Rev.
Virol.
2, 135–159.
4.
Young , GR, Eksmond, U.
, Salcedo, R.
, Alexopoulou, L.
, Stoye, JP, and Kassiotis, G.
(2012a).
Resurrection of endogenous retroviruses in antibody-deficient mice.
Nature 491, 774-778.
[Original Articles] BioArt original articles are welcome to be shared by individuals.
Reprinting is prohibited without permission.
The copyrights of all published works are owned by BioArt
.
BioArt reserves all statutory rights and offenders must be investigated
.
.
It has been reported that the microbiota exposed on the skin surface can promote the accumulation of various lymphocyte subpopulations in the skin, thereby promoting tissue repair [1]
.
However, it is not clear how the immune system actively recognizes and responds to the microbiota in the absence of typical inflammatory processes
.
Interestingly, the microbiota can promote IFN-I production and antiviral status in tissues.
These findings seem to suggest that the microbiota can protect the host from viral infections [2]
.
Retroviruses can integrate as part of the host genome
.
Therefore, the long-term symbiotic relationship between mammals and microorganisms includes not only exogenous microorganisms (such as bacteria, fungi, and viruses), but also symbiotic relationships with endogenous retroviruses (ERVs) [3]
.
Most ERVs are in an inactive state; however, there are several ERVs expressing complete open reading frames, and their transcriptional activity is related to various physiological and pathological processes, so they are under constant immune pressure
.
Previous reports suggested that in some cases, microbial exposure can control the expression of ERVs [4], however, whether ERVs are directly involved in inducing responses to the microbiota is still unknown
.
In addition, under certain circumstances, the extent to which the high expression of ERVs may cause the inflammatory effects of the microbiota has not been resolved
.
On June 23, 2021, the Yasmine Belkaid team from the National Institutes of Health published an article entitled Endogenous retroviruses promote homeostatic and inflammatory responses to the microbiota in Cell.
In this study, the author proposed skin microbes Population can promote the expression of ERVs, and the intrinsic response of keratinocytes to ERVs depends on cGAS/STING signal transduction, and at the same time promotes the induction of T cells
.
If the reverse transcription of ERVs is inhibited, the microbial immune response and related tissue repair function will be impaired, and the high-fat diet can increase the expression of ERVs, which in turn leads to increased immune response and tissue inflammation
.
In summary, studies have shown that the host immune system uses the endogenous virus group to interact with the exogenous microbiota to regulate tissue repair or inflammation
.
The skin colonization of symbiotic bacteria often promotes the accumulation of various T cell subgroups in the skin in a way that is not coupled with the inflammatory process
.
For example, in the absence of tissue inflammation, mice with Staphylococcus epidermidis colonized on the skin surface are significantly up-regulated compared to SFP mice, many genes related to immune activation, among which are related to IFN-I and antiviral response The up-regulation of genes is the most obvious
.
It should be noted that previous reports pointed out that the induction of ERVs is related to the induction of IFN-I response, and the presence of Staphylococcus epidermidis is promoting the expression of several endogenous reverse transcription factor families
.
Next, the authors used mice treated with a combination of reverse transcriptase inhibitors to evaluate whether the cDNA synthesis of endogenous reverse transcriptase elements controls the T cell response to Staphylococcus epidermidis
.
Skin imaging shows that antiretroviral treatment can significantly inhibit the accumulation of T cells in the epidermis, and it can also significantly reduce the expression of IL-17 in CD8+, MAIT and γδ T cells in the skin
.
At the same time, scRNA-seq showed that this treatment also affected gene expression programs related to antibacterial defense and tissue repair
.
So what are the DNA sensors that may be involved in these reactions? Previous evidence has shown that retroviruses can activate cGAS to produce cGAMP, which further activates STING
.
Based on this, the authors verified that the absence of STING in keratinocytes can significantly reduce the number of all T cell subsets and the production of related cytokines
.
Although homeostasis of the microbiota promotes immune adaptability, conversely, the disorders of these symbiotic bacteria can also promote tissue inflammation
.
To test the possibility that ERVs may cause pathogenic effects on the microbiota, the authors used an intervention model that uses a high-fat diet to promote inflammation
.
Interestingly, there was no inflammation in the epidermis of mice on a normal diet, while epidermal hyperplasia and hyperkeratinization were significantly increased in mice on a high-fat diet.
At the same time, it was accompanied by high expression of inflammation-related genes and a variety of ERVs families
.
However, cGas-/-, Sting-/-, Ifnar1-/- mice have significantly reduced skin inflammation and epidermal hyperplasia under high-fat diet, confirming that the cGAS/STING/IFN-I axis is involved in the metabolism of the microbiota The ability to promote inflammation under changing circumstances
.
These findings are not only applicable to mouse models.
In order to evaluate this potential correlation with human skin inflammation, the authors also analyzed skin samples from psoriasis patients in this study.
The results showed that reverse transcription in psoriasis skin lesions The enzyme locus is strongly induced relative to normal skin, which means that skin inflammation in mice and humans may be related to the enhanced expression of ERVs
.
In general, this study puts forward the view that the host may choose the endogenous virus group as a means of communicating with the exogenous microbiota, and the immune response to the microbiota under steady-state immunity and inflammation.
The degree of ERVs is controlled by the expression of ERVs.
Therefore, the response of ERVs to microorganisms should be integrated into our understanding of diseases and inflammatory states
.
Original link: https://doi.
org/10.
1016/j.
cell.
2021.
05.
020 Platemaker: 11 References 1.
Belkaid, Y.
, and Harrison, OJ (2017).
Homeostatic immunity and the microbiota.
Immunity 46 , 562–576.
2.
Abt, MC, Osborne, LC, Monticelli, LA, Doering, TA, Alenghat, T.
, Sonnenberg, GF, Paley, MA, Antenus, M.
, Williams, KL, Erikson, J.
, et al .
(2012).
Commensal bacteria calibrate the activation threshold of innate antiviral immunity.
Immunity 37, 158–170.
3.
Johnson, WE (2015).
Endogenous retroviruses in the genomics era.
Annu.
Rev.
Virol.
2, 135–159.
4.
Young , GR, Eksmond, U.
, Salcedo, R.
, Alexopoulou, L.
, Stoye, JP, and Kassiotis, G.
(2012a).
Resurrection of endogenous retroviruses in antibody-deficient mice.
Nature 491, 774-778.
[Original Articles] BioArt original articles are welcome to be shared by individuals.
Reprinting is prohibited without permission.
The copyrights of all published works are owned by BioArt
.
BioArt reserves all statutory rights and offenders must be investigated
.
