The genome is constantly facing challenges from genotoxic agents and physiological DNA breaks. To deal with these DNA lesions, the cells evolve several sets of DNA repair machinery to precisely and timely repair the DNA damage, thereby maintaining the genome integrity. Defective DNA repair will lead to aberrancies including tumorigeneses and genetic disorders including immunodeficiency. DNA double-strand breaks (DSBs) are particularly lethal lesions, which activate the canonical DNA damage response (cDDR) in cells. The cDDR is initiated by three PI3K-like protein kinases: DNA-PKcs, ATM, and ATR. The DSBs are then repaired either through Non-Homologous End Joining (NHEJ) or Homologous Recombination (HR) tightly regulated by these kinases.
The DSBs generated in immune cells regulate their development and functions. Programmed DSBs at specific genomic locations in adaptive immune cells are required for assembly of antigen receptor gene by V(D)J recombination, immunoglobulin class switch recombination (CSR), and other processes. Moreover, non-programmed DSB generated during transcription, replication, or pathogen eradication in immune cells are also implicated in regulating their development and functions. Though the links between DNA repair machinery and immune diversity are established, much more information is under the tip of the iceberg.
Expanding evidence has shown the connection between DNA repair machinery and nucleic acid sensing pathways such as cGAS-STING. The nucleic acid sensing process is not only critical for innate immune cells to orchestrate the innate and adaptive immunity against viral infection or tumor, but also one of the determining factors for tumor immunotherapy. Several DNA repair factors are involved in the processing or sensing of cytosolic nucleic acids. On the other side, the nucleic acid sensing pathways also show impacts on the DNA repair in the nucleus. Therefore, much deeper cross-talks between DNA repair machinery and the nucleic acid sensing pathways need further elucidation to better treat diseases such as infectious diseases or cancer.
For this Research Topic, we are interested in Original Research articles, Review articles, Mini Review articles, and Brief Research Report articles that focus on the following topics:
1. Crosstalk between DNA repair machinery and nucleic acid sensing in innate immunity.
2. Role of DNA repair factors in the regulation of antigen receptor diversification including V(D)J recombination, Somatic Hypermutation, Class Switch Recombination, and gene conversion.
3. Novel DNA repair proteins or pathways in lymphocyte development and immune response.
4. The DNA damage response and DNA repair pathways in lymphocytes after radiation or in the tumor microenvironment after radiotherapy.
The genome is constantly facing challenges from genotoxic agents and physiological DNA breaks. To deal with these DNA lesions, the cells evolve several sets of DNA repair machinery to precisely and timely repair the DNA damage, thereby maintaining the genome integrity. Defective DNA repair will lead to aberrancies including tumorigeneses and genetic disorders including immunodeficiency. DNA double-strand breaks (DSBs) are particularly lethal lesions, which activate the canonical DNA damage response (cDDR) in cells. The cDDR is initiated by three PI3K-like protein kinases: DNA-PKcs, ATM, and ATR. The DSBs are then repaired either through Non-Homologous End Joining (NHEJ) or Homologous Recombination (HR) tightly regulated by these kinases.
The DSBs generated in immune cells regulate their development and functions. Programmed DSBs at specific genomic locations in adaptive immune cells are required for assembly of antigen receptor gene by V(D)J recombination, immunoglobulin class switch recombination (CSR), and other processes. Moreover, non-programmed DSB generated during transcription, replication, or pathogen eradication in immune cells are also implicated in regulating their development and functions. Though the links between DNA repair machinery and immune diversity are established, much more information is under the tip of the iceberg.
Expanding evidence has shown the connection between DNA repair machinery and nucleic acid sensing pathways such as cGAS-STING. The nucleic acid sensing process is not only critical for innate immune cells to orchestrate the innate and adaptive immunity against viral infection or tumor, but also one of the determining factors for tumor immunotherapy. Several DNA repair factors are involved in the processing or sensing of cytosolic nucleic acids. On the other side, the nucleic acid sensing pathways also show impacts on the DNA repair in the nucleus. Therefore, much deeper cross-talks between DNA repair machinery and the nucleic acid sensing pathways need further elucidation to better treat diseases such as infectious diseases or cancer.
For this Research Topic, we are interested in Original Research articles, Review articles, Mini Review articles, and Brief Research Report articles that focus on the following topics:
1. Crosstalk between DNA repair machinery and nucleic acid sensing in innate immunity.
2. Role of DNA repair factors in the regulation of antigen receptor diversification including V(D)J recombination, Somatic Hypermutation, Class Switch Recombination, and gene conversion.
3. Novel DNA repair proteins or pathways in lymphocyte development and immune response.
4. The DNA damage response and DNA repair pathways in lymphocytes after radiation or in the tumor microenvironment after radiotherapy.
