scholarly journals Toll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Wenjin Zheng ◽  
Qing Xu ◽  
Yiyuan Zhang ◽  
Xiaofei E ◽  
Wei Gao ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Signaling Pathways ◽  
Critical Role ◽  
Innate Immune ◽  
Host Cells ◽  
Main Body ◽  
Current Perspective ◽  
Viral Components

Abstract Background In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. Main body Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against herpesviridae, and systematically describes the processes of TLR actions and herpesviridae recognition as well as the signal transduction pathways involved. Conclusions Future studies of the interactions between TLRs and herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.

A Critical Role for Innate Immunity In Allogeneic Hematopoietic Cell Rejection Via the TLR4/TRIF Pathway

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 77-77
Author(s):  
Hong Xu ◽  
Jun Yan ◽  
Ziqiang Zhu ◽  
Yiming Huang ◽  
Yujie Wen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Innate Immunity ◽  
T Cells ◽  
Immune System ◽  
T Cell ◽  
Innate Immune System ◽  
Critical Role ◽  
Innate Immune ◽  
Wild Type

Abstract Abstract 77 Adaptive immunity, especially T cells, has long been believed to be the dominant immune barrier in allogeneic transplantation. Targeting host T cells significantly reduces conditioning for bone marrow cell (BMC) engraftment. Innate immunity has been recently shown to pose a significant barrier in solid organ transplantation, but has not been addressed in bone marrow transplantation (BMT). Using T cell deficient (TCR-β/δ−/−) or T and B cell deficient (Rag−/−) mice, we found that allogeneic BMC rejection occurred early before the time required for T cell activation and was T- and B-cell independent, suggesting an effector role for innate immune cells in BMC rejection. Therefore, we hypothesized that by controlling both innate and adaptive immunity, the donor BMC would have a window of advantage to engraft. Survival of BMC in vivo was significantly improved by depleting recipient macrophages and/or NK cells, but not neutrophils. Moreover, depletion of macrophages and NK cells in combination with co-stimulatory blockade with anti-CD154 and rapamycin as a novel form of conditioning resulted in 100% allogeneic engraftment without any irradiation and T cell depletion. Donor chimerism remained stable and durable up to 6 months. Moreover, specific Vβ5½ and Vβ11 clonal deletion was detected in host CD4+ T cells in chimeras, indicating central tolerance to donor alloantigens. Whether and how the innate immune system recognizes or responds to allogeneic BMCs remains unknown. Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. The signaling function of TLR depends on intracellular adaptors. The adaptor MyD88 transmits signals emanating from all TLR, except TLR3 while TRIF specifically mediates TLR3 and TLR4 signaling via type 1 IFN. To further determine the innate signaling pathways in allogeneic BMC rejection, B6 background (H2b) MyD88−/− and TRIF−/− mice were conditioned with anti-CD154/rapamycin plus 100 cGy total body irradiation and transplanted with 15 × 106 BALB/c (H2d) BMC. Only 33.3% of MyD88−/− recipients engrafted at 1 month, resembling outcomes for wild-type B6 mice. In contrast, 100% of TRIF−/− mice engrafted. The level of donor chimerism in TRIF−/− mice was 5.1 ± 0.6% at one month, significantly higher than in MyD88−/− and wild-type B6 controls (P < 0.005). To determine the mechanism of innate signaling in BMC rejection, we examined whether TRIF linked TLR3 or TLR4 is the key pattern recognition receptor involved in BMC recognition. To this end, TLR3−/− and TLR4−/− mice were transplanted with BALB/c BMC with same conditioning. None of the TLR3−/− mice engrafted. In contrast, engraftment was achieved in 100% of TLR4−/− mice up to 6 months follow up. Taken together, these results suggest that rejection of allogeneic BMC is uniquely dependent on the TLR4/TRIF signaling pathway. Thus, our results clearly demonstrate a previously unappreciated role for innate immunity in allogeneic BMC rejection. Our current findings are distinct from prior reports demonstrating a critical role of MyD88 in rejection of allogeneic skin grafts and lung, and may reflect unique features related to BMC. The findings of the role of innate immunity in BMC rejection would lead to revolutionary changes in our understanding and management of BMT. This would be informative in design of more specific innate immune targeted conditioning proposals in BMT to avoid the toxicity. Disclosures: Bozulic: Regenerex LLC: Employment. Ildstad:Regenerex LLC: Equity Ownership.

scholarly journals IRF1 Promotes the Innate Immune Response to Viral Infection by Enhancing the Activation of IRF3

2020 ◽  
Vol 94 (22) ◽  
Author(s):  
Jingjing Wang ◽  
Huiyi Li ◽  
Binbin Xue ◽  
Rilin Deng ◽  
Xiang Huang ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Critical Role ◽  
Innate Immune ◽  
Host Cells ◽  
Functional Domain ◽  
Phosphatase 2A

ABSTRACT Innate immunity is an essential way for host cells to resist viral infection through the production of interferons (IFNs) and proinflammatory cytokines. Interferon regulatory factor 3 (IRF3) plays a critical role in the innate immune response to viral infection. However, the role of IRF1 in innate immunity remains largely unknown. In this study, we found that IRF1 is upregulated through the IFN/JAK/STAT signaling pathway upon viral infection. The silencing of IRF1 attenuates the innate immune response to viral infection. IRF1 interacts with IRF3 and augments the activation of IRF3 by blocking the interaction between IRF3 and protein phosphatase 2A (PP2A). The DNA binding domain (DBD) of IRF1 is the key functional domain for its interaction with IRF3. Overall, our study reveals a novel mechanism by which IRF1 promotes the innate immune response to viral infection by enhancing the activation of IRF3, thereby inhibiting viral infection. IMPORTANCE The activation of innate immunity is essential for host cells to restrict the spread of invading viruses and other pathogens. IRF3 plays a critical role in the innate immune response to RNA viral infection. However, whether IRF1 plays a role in innate immunity is unclear. In this study, we demonstrated that IRF1 promotes the innate immune response to viral infection. IRF1 is induced by viral infection. Notably, IRF1 targets and augments the phosphorylation of IRF3 by blocking the interaction between IRF3 and PP2A, leading to the upregulation of innate immunity. Collectively, the results of our study provide new insight into the regulatory mechanism of IFN signaling and uncover the role of IRF1 in the positive regulation of the innate immune response to viral infection.

Biogenic particles can be multiantigenic, immunostimulative and activate innate immunity while suppressing tumor development

2021 ◽  
Author(s):  
Moataz Dowaidar
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Cancer Immunotherapy ◽  
Cancer Vaccines ◽  
Tumor Antigens ◽  
Critical Role ◽  
Tumor Development ◽  
Host Cells ◽  
Delivery Technique ◽  
Biogenic Nanoparticles

Cancer immunotherapy, which attempts to activate or stimulate the immune system to treat cancer, has become the standard of treatment. Although some cancer vaccines are efficiently translated, they have not yet reached the same degree of success as infectious disease immunizations. A primary factor is the low immunogenicity of the tumor and related antigens. Unlike viruses, cancer cells emerge from somatic mutations in patients' healthy tissues, making it harder for the immune system to properly detect tumor cells. Biogenic nanoparticles have recently been highlighted as a solution to address some of the issues with creating anticancer vaccinations. Antigens, medication delivery, and others all benefit from biogenic nanoparticles. Biogenic nanoparticles have long been researched as a vaccine. Biogenic nanoparticles-based platforms, like particular VLPs, inherently activate inflammatory responses and may be increased with TAAs evaluated for antigen-specific antitumor responses to patient malignancies. OMVs and OMV-coated nanoparticles can be multiantigenic and immunostimulative in the box. PAMPs present in OMVs can activate innate immunity while suppressing tumor development. A range of cells, including immune and malignant cells, produce exosomes and play a critical role in cell-to-cell communication. Exosomes may contain interesting materials such as specific drugs, proteins, DNA, and RNA species, and their function depends on host cells. In cancer vaccines, however, these biogenic nanoparticles still have some limitations. Transferring tumor antigens and adjuvants to the secondary lymphoid system is a critical issue for biogenic nanoparticles. OMVs lack tumor antigens. Adjuvants are low in VLPs and exosomes. Furthermore, enhancing the protective response of biogenic nanoparticles, generating protective antigens in these nanoparticles and reducing the toxicity of nanoparticles are all challenges in cancer immunotherapy. There has been a lot of information regarding biogenic nanoparticles created by a variety of bacteria or cells in the area of bacterial vesicle research for a long time, but there has been a dearth of in-depth study focused on identifying molecules crucial to biogenesis or biogenic nanoparticles. Many basic questions remain unanswered here. Which envelope factors release biogenic nanoparticles? What signals and mechanisms regulate biogenic biogenic nanoparticles? Understanding these and other concepts as a cancer immunotherapy delivery technique is vital for the future development of biogenic nanoparticles. Future investigations are anticipated to begin to address these fundamental issues and increase our knowledge.

scholarly journals Guanylate-Binding Protein 1 Inhibits Nuclear Delivery of Kaposi's Sarcoma-Associated Herpesvirus Virions by Disrupting Formation of Actin Filament

2017 ◽  
Vol 91 (16) ◽  
Author(s):  
Zhe Zou ◽  
Zhihua Meng ◽  
Chao Ma ◽  
Deguang Liang ◽  
Rui Sun ◽  
...  
Keyword(s):  
Immune System ◽  
Actin Filaments ◽  
Primary Infection ◽  
Rna Viruses ◽  
Critical Role ◽  
Host Cells ◽  
Host Immune System ◽  
Kshv Infection ◽  
Guanylate Binding Protein

ABSTRACT Kaposi's sarcoma-associated herpesvirus (KSHV) is a typical gammaherpesvirus that establishes persistent lifelong infection in host cells. In order to establish successful infection, KSHV has evolved numerous immune evasion strategies to bypass or hijack the host immune system. However, host cells still produce immune cytokines abundantly during primary KSHV infection. Whether the immune effectors produced are able to inhibit viral infection and how KSHV successfully conquers these immune effectors remain largely unknown. The guanylate-binding protein 1 (GBP1) gene is an interferon-stimulated gene and exerts antiviral functions on several RNA viruses; however, its function in DNA virus infection is less well understood. In this study, we found that KSHV infection increases both the transcriptional and protein levels of GBP1 at the early stage of primary infection by activating the NF-κB pathway. The overexpression of GBP1 significantly inhibited KSHV infection, while the knockdown of GBP1 promoted KSHV infection. The GTPase activity and dimerization of GBP1 were demonstrated to be responsible for its anti-KSHV activity. Furthermore, we found that GBP1 inhibited the nuclear delivery of KSHV virions by disrupting the formation of actin filaments. Finally, we demonstrated that replication and transcription activator (RTA) promotes the degradation of GBP1 through a proteasome pathway. Taken together, these results provide a new understanding of the antiviral mechanism of GBP1, which possesses potent anti-KSHV activity, and suggest the critical role of RTA in the evasion of the innate immune response during primary infection by KSHV. IMPORTANCE GBP1 can be induced by various cytokines and exerts antiviral activities against several RNA viruses. Our study demonstrated that GBP1 can exert anti-KSHV function by inhibiting the nuclear delivery of KSHV virions via the disruption of actin filaments. Moreover, we found that KSHV RTA can promote the degradation of GBP1 through a proteasome-mediated pathway. Taken together, our results elucidate a novel mechanism of GBP1 anti-KSHV activity and emphasize the critical role of RTA in KSHV evasion of the host immune system during primary infection.

scholarly journals Role of Intestinal Alkaline Phosphatase in Innate Immunity

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1784
Author(s):  
Sudha B. Singh ◽  
Henry C. Lin
Keyword(s):  
Innate Immunity ◽  
Alkaline Phosphatase ◽  
Critical Role ◽  
Host Cells ◽  
Immune Functions ◽  
Intestinal Alkaline Phosphatase ◽  
Functional Protein ◽  
Mammalian Cell Lines ◽  
Defensive Role

Intestinal alkaline phosphatase (IAP) is a multi-functional protein that has been demonstrated to primarily protect the gut. The role of IAP in maintaining intestinal homeostasis is underscored by the observation that IAP expression is defective in many gastrointestinal-related disorders such as inflammatory bowel disease IBD, necrotizing enterocolitis, and metabolic syndrome and that exogenous IAP supplementation improves the outcomes associated with these disorders. Additionally, studies using transgenic IAP-knock out (IAP-KO) mouse models further support the importance of the defensive role of IAP in the intestine. Supplementation of exogenous IAP and cellular overexpression of IAP have also been used in vitro to dissect out the downstream mechanisms of this protein in mammalian cell lines. Some of the innate immune functions of IAP include lipopolysaccharide (LPS) detoxification, protection of gut barrier integrity, regulation of gut microbial communities and its anti-inflammatory roles. A novel function of IAP recently identified is the induction of autophagy. Due to its critical role in the gut physiology and its excellent safety profile, IAP has been used in phase 2a clinical trials for treating conditions such as sepsis-associated acute kidney injury. Many excellent reviews discuss the role of IAP in physiology and pathophysiology and here we extend these to include recent updates on this important host defense protein and discuss its role in innate immunity via its effects on bacteria as well as on host cells. We will also discuss the relationship between IAP and autophagy and how these two pathways may act in concert to protect the gut.

scholarly journals Mismatch in Sirpα, a Regulatory Protein in Innate Immunity, Is Associated with Outcomes of Allogeneic Stem Cell Transplantation for Lymphoid Malignancies

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1804-1804
Author(s):  
Rima M. Saliba ◽  
Uri Greenbaum ◽  
Qing Ma ◽  
Samer A. Srour ◽  
Gabriela Rondon ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Stem Cell ◽  
Immune System ◽  
Acute Gvhd ◽  
Lymphoblastic Leukemia ◽  
Regulatory Protein ◽  
Innate Immune ◽  
Lymphoid Malignancies ◽  
Related Donor

Abstract Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a potentially curative therapy for patients with hematologic malignancies. It is conventionally believed that alloreactivity is initiated by T-cells recognizing the non-self HLA molecules on the graft. Cells from the innate immune system, such as macrophages and monocytes, are induced by nonspecific "danger" molecules released from damaged tissue. Recent studies revealed that the innate immune system could distinguish the non-self graft and subsequently prime the adaptive immune system to advance the allorecognition process. Signal regulatory protein α (SIRPα) is an immunoglobulin superfamily receptor that is expressed on macrophages and myeloid cells. The interaction between SIRPα and its ubiquitously expressed ligand, CD47, suppresses the macrophages phagocytic function. It has been demonstrated that recipient's monocytes detect polymorphism in SIRPα, and mismatches of SIRPα between donor and recipient can regulate the allorecognition response in the murine model. Our group has recently investigated the role of SIRPα variant mismatch in recipients of allo-HSCT from an HLA-matched related donor for treatment of acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). We found that donor/recipient SIRPα mismatch was commonly detected in 39% of transplant pairs, and the presence of the mismatch was significantly associated with an increase rate of chronic graft-versus-host disease (cGvHD) and a lower rate of early relapse. We hypothesized that comparable effects could be occurring in recipients of allo-HSCT for treatment of lymphoid malignancies. We tested our hypothesis in a cohort of patients who received an allo-HSCT from an HLA matched-related donor at our institution between January 2008 and December 2018 for the treatment of lymphoid malignancies. Only patients who received a peripheral blood stem cell graft and tacrolimus/methotrexate for GvHD prophylaxis were eligible for the study. A total of 313 patients met the eligibility criteria including 310 (99%) who engrafted and 3 (1%) who died early before engraftment. The risk of early death was not associated with SIRPα mismatch variant. Only patients who engrafted (N=310) were included in subsequent analyses. Among these, 42% (N=130) of donor/recipient pairs were SIRPα mismatched. The majority of patients were treated for acute lymphoblastic leukemia (N=115, 37%) or non-Hodgkin's lymphoma (NHL) (N=114, 37%), followed by chronic lymphoblastic leukemia (N=59, 19%), and Hodgkin's lymphoma (N=22, 7%). Most (N=259, 84%) of patients had chemo-sensitive disease. The median age at transplant was 51 (range: 18-72) years, and 64% of patients were female. The median age of donors was 50 (range: 18-79) years and 53% were male. Conditioning regimens were myeloablative in 52% of cases. Outcomes were evaluated accounting for competing risks. The median follow-up in surviving patients was 74 (range: 3-124) months. A total of 99, 84, 108, and 51 patients experienced grade 2-4 acute GvHD, cGvHD requiring systemic immunosuppressive therapy, disease progression, and non-relapse mortality (NRM), respectively. Multivariate analyses showed that SIRPα mismatch was associated with a significantly higher rate (hazard ratio [HR]=1.9, P=.005) of cGvHD requiring systemic immunosuppressive therapy, and a lower rate (HR=.5, P=.004) of disease progression. Notably, the increased rate of cGVHD was consistent across the 4 lymphoid malignancies evaluated, yet the lower rate of relapse was observed in all diagnoses except NHL. There was no significant impact of SIRPα mismatch on grade 2-4 acute GvHD (HR=1.2, P=.3) or on NRM (HR=0.7, P=.3). Consistent with our preceding study in the AML/MDS cohort, the mismatch in SIRPα, a regulatory protein in innate immunity, is associated with a higher rate of cGvHD and relapse protection in patients who underwent allo-HSCT for lymphoid malignancies. The results of this study could be clinically important in donor selection and provide insight into the underlying role of innate immunity in allo-HSCT. Disclosures Shpall: Adaptimmune: Consultancy; Takeda: Patents & Royalties; Novartis: Consultancy; Magenta: Honoraria; Navan: Consultancy; Bayer HealthCare Pharmaceuticals: Honoraria; Magenta: Consultancy; Axio: Consultancy; Affimed: Patents & Royalties; Novartis: Honoraria.

Innate immune receptors in type 1 diabetes: the relationship to cell death-associated inflammation

2020 ◽  
Vol 48 (3) ◽  
pp. 1213-1225 ◽  
Author(s):  
Tae Kang Kim ◽  
Myung-Shik Lee
Keyword(s):  
Innate Immunity ◽  
Type 1 Diabetes ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Innate Immune ◽  
Therapeutic Modalities ◽  
Immune Receptors ◽  
Molecular Patterns

The importance of innate immunity in host defense and inflammatory responses has been clearly demonstrated after the discovery of innate immune receptors such as Toll-like receptors (TLRs) or Nucleotide-binding oligomerization domain-containing protein (Nod)-like receptors (NLRs). Innate immunity also plays a critical role in diverse pathological conditions including autoimmune diseases such as type 1 diabetes (T1D). In particular, the role of a variety of innate immune receptors in T1D has been demonstrated using mice with targeted disruption of such innate immune receptors. Here, we discuss recent findings showing the role of innate immunity in T1D that were obtained mostly from studies of genetic mouse models of innate immune receptors. In addition, the role of innate immune receptors involved in the pathogenesis of T1D in sensing death-associated molecular patterns (DAMPs) released from dead cells or pathogen-associated molecular patterns (PAMPs) will also be covered. Elucidation of the role of innate immune receptors in T1D and the nature of DAMPs sensed by such receptors may lead to the development of new therapeutic modalities against T1D.

T6SS translocates a micropeptide to suppress STING-mediated innate immunity by sequestering manganese

2021 ◽  
Vol 118 (42) ◽  
pp. e2103526118
Author(s):  
Lingfang Zhu ◽  
Lei Xu ◽  
Chenguang Wang ◽  
Changfu Li ◽  
Mengyuan Li ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Metal Ions ◽  
Innate Immune Response ◽  
Metal Ion ◽  
Innate Immune ◽  
Host Cells ◽  
Host Innate Immune Response ◽  
Host Innate Immunity

Cellular ionic concentrations are a central factor orchestrating host innate immunity, but no pathogenic mechanism that perturbs host innate immunity by directly targeting metal ions has yet been described. Here, we report a unique virulence strategy of Yersinia pseudotuberculosis (Yptb) involving modulation of the availability of Mn2+, an immunostimulatory metal ion in host cells. We showed that the Yptb type VI secretion system (T6SS) delivered a micropeptide, TssS, into host cells to enhance its virulence. The mutant strain lacking TssS (ΔtssS) showed substantially reduced virulence but induced a significantly stronger host innate immune response, indicating an antagonistic role of this effector in host antimicrobial immunity. Subsequent studies revealed that TssS is a Mn2+-chelating protein and that its Mn2+-chelating ability is essential for the disruption of host innate immunity. Moreover, we showed that Mn2+ enhances the host innate immune response to Yptb infection by activating the stimulator of interferon genes (STING)-mediated immune response. Furthermore, we demonstrated that TssS counteracted the cytoplasmic Mn2+ increase to inhibit the STING-mediated innate immune response by sequestering Mn2+. Finally, TssS-mediated STING inhibition sabotaged bacterial clearance in vivo. These results reveal a previously unrecognized bacterial immune evasion strategy involving modulation of the bioavailability of intracellular metal ions and provide a perspective on the role of the T6SS in pathogenesis.

scholarly journals Innate Pathways of Immune Activation in Transplantation

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Todd V. Brennan ◽  
Keri E. Lunsford ◽  
Paul C. Kuo
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Critical Role ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Immune Recognition ◽  
First Line ◽  
Adaptive Immune

Studies of the immune mechanisms of allograft rejection have predominantly focused on the adaptive immune system that includes T cells and B cells. Recent investigations into the innate immune system, which recognizes foreign antigens through more evolutionarily primitive pathways, have demonstrated a critical role of the innate immune system in the regulation of the adaptive immune system. Innate immunity has been extensively studied in its role as the host's first-line defense against microbial pathogens; however, it is becoming increasingly recognized for its ability to also recognize host-derived molecules that result from tissue damage. The capacity of endogenous damage signals acting through the innate immune system to lower immune thresholds and promote immune recognition and rejection of transplant grafts is only beginning to be appreciated. An improved understanding of these pathways may reveal novel therapeutic targets to decrease graft alloreactivity and increase graft longevity.

scholarly journals The Critical Role of Small RNAs in Regulating Plant Innate Immunity

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 184
Author(s):  
Saquib Waheed ◽  
Muhammad Anwar ◽  
Muhammad Asif Saleem ◽  
Jinsong Wu ◽  
Muhammad Tayyab ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Small Rnas ◽  
Plant Immunity ◽  
Critical Role ◽  
Innate Immune ◽  
Genes Encoding ◽  
Effector Triggered Immunity ◽  
Available Information ◽  
Regulatory Functions

Plants, due to their sessile nature, have an innate immune system that helps them to defend against different pathogen infections. The defense response of plants is composed of a highly regulated and complex molecular network, involving the extensive reprogramming of gene expression during the presence of pathogenic molecular signatures. Plants attain proper defense against pathogens through the transcriptional regulation of genes encoding defense regulatory proteins and hormone signaling pathways. Small RNAs are emerging as versatile regulators of plant development and act in different tiers of plant immunity, including pathogen-triggered immunity (PTI) and effector-triggered immunity (ETI). The versatile regulatory functions of small RNAs in plant growth and development and response to biotic and abiotic stresses have been widely studied in recent years. However, available information regarding the contribution of small RNAs in plant immunity against pathogens is more limited. This review article will focus on the role of small RNAs in innate immunity in plants.

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