Neutrophils in rheumatoid arthritis: More than simple final effectors (2022)

Table of Contents
Autoimmunity Reviews Abstract Introduction Section snippets Immune mediators production Conclusion Take-home messages Acknowledgments References (40) Am J Pathol Int J Biochem Cell Biol FEBS Lett J Autoimmun J Autoimmun Cell Immunol J Autoimmun Autoimmun Rev Blood Neutrophils and immunity: challenges and opportunities Nat Rev Immunol Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing Nat Med Secretion of oncostatin M by neutrophils in rheumatoid arthritis Arthritis Rheum Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis Arthritis Res Ther Expression of vascular endothelial growth factor by synovial fluid neutrophils in rheumatoid arthritis (RA) Clin Exp Immunol Elevated serum B lymphocyte stimulator levels in patients with systemic immune-based rheumatic diseases Arthritis Rheum Tumor necrosis factor alpha activates release of B lymphocyte stimulator by neutrophils infiltrating the rheumatoid joint Arthritis Rheum Citrullination of synovial proteins in murine models of rheumatoid arthritis Arthritis Rheum Granulocyte colony-stimulating factor and neutrophils—forgotten mediators of inflammatory disease Nat Clin Pract Rheumatol Phagocyte-derived reactive oxygen species as suppressors of inflammatory disease Arthritis Rheum Enhanced inflammatory responses of chronic granulomatous disease leukocytes involve ROS-independent activation of NF-kappa B Eur J Immunol Cited by (159) Recommended articles (6) FAQs Videos

RegisterSign in


  • Access throughyour institution

Autoimmunity Reviews

Volume 9, Issue 8,

June 2010

, Pages 531-535


Rheumatoid arthritis is the most common inflammatory joint disease. The etiopathogenesis of this condition has been classically explained by a T cell-driven process. However, recent studies have highlighted the possible contribution of neutrophils for the early phases of RA physiopathology. These cells are phagocytic leukocytes that play crucial roles in the acute defense against pathogens while modulating the function of other immune cells and contributing to the perpetuation of an initial inflammatory response. The herein article reviews recent progresses in the understanding of the immunopathology of RA with a special emphasis on the role of neutrophils.


Rheumatoid arthritis (RA) is a chronic immune inflammatory disease characterized by synovial hyperplasia, joint destruction and extra-articular manifestations with a significant impact on both morbidity and mortality. Although the etiopathology of this condition is not fully understood, it is known that neutrophils, macrophages, synovial fibroblasts, T cells and B cells are involved in the mechanisms that drive the onset of RA. T cells, B cells and macrophages infiltrate the synovium and form discrete lymphoid aggregates, sometimes with ectopic germinal centers, while macrophage-like and fibroblast-like synoviocytes accumulate in the intima causing hyperplasia and secreting degradative enzymes. However, before these events take place, neutrophils migrate to the synovial fluid (SF) where they phagocyte immune complexes and release powerful proteases. Neutrophils, which are part of the innate immunity, are crucial for pathogenic defense. They are the first cell type to arrive at sites of inflammation, followed by monocytes [1]. In a normal inflammatory response and upon appropriate stimuli, neutrophils are able to release cytotoxic mediators, such as reactive oxygen (ROS) and nitrogen (RNS) species and proteases into the extracellular space, generating damage to the pathogen and to the host tissues. Consequently, and after elimination of the pro-inflammatory stimulus, there is an urgent need to repair the injuries and return to a state of homeostasis. This is manifested as a shift towards anti-inflammatory signals that ultimately lead to the resolution of inflammation. At this point, neutrophils must die by apoptosis and be ingested by macrophages that are involved in clearing the inflamed area. Concomitantly, anti-inflammatory signals such as macrophage-derived lipoxins stop the influx of neutrophils and activate macrophages to phagocyte dead cells, thus pushing the inflammatory response towards resolution of inflammation [2]. In RA the mechanisms of neutrophil activation, recruitment and apoptosis are altered. This review is focused on recent developments in the immunobiology of RA, specifically regarding the contribution of neutrophils for disease progression.

Section snippets

Immune mediators production

Mature neutrophils have been considered terminally differentiated cells that have a low level of de novo protein synthesis. However, neutrophils were shown to synthesize a large variety of cytokines and chemokines under inflammatory conditions. Although neutrophils produce lower amounts of these molecules than other cells, their higher number at inflammatory sites makes them an important source for these proteins. Cytokines and chemokines are crucial to amplify inflammation, by recruiting more


The traditional concept of the neutrophil as a professional phagocytic cell only able to destroy pathogens and tissues seems to be at odds with recently obtained data. Neutrophils in chronic inflammatory settings, as is the case of RA, are able to interact with other cells and to regulate their functions. They produce inflammatory mediators that contribute to the regulation of the inflammatory process and are able to adopt different phenotypes like APC or osteoclasts. In summary, neutrophils

Take-home messages

Neutrophils are the first cell type to arrive at sites of inflammation.

Under chronic inflammatory conditions neutrophils are able to release protease-rich granules and to produce high amounts of ROS.

Neutrophils secrete immune mediators which can activate themselves and other immune cells, triggering positive regulatory feedbacks which lead to acute and persistent inflammation.

Neutrophils live longer in inflammatory sites, augmenting the release of powerful destructive enzymes.

Neutrophils are


This work was supported by a fellowship from Fundação para a Ciência e a Tecnologia (FCT) SFRH/BD/40513/2007 and partially supported by a grant from Sociedade Portuguesa de Reumatologia and FCT grant PTDC/SAU-OSM/73449/2006.

(Video) Neutrophil Contribution to Inflammation and Autoimmunity in Rheumatic Disease

References (40)

  • G.S. Ashcroft et al.

    Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing

    Nat Med


    (Video) Neutrophils in Inflammation and Autoimmunity

  • A. Cross et al.

    Secretion of oncostatin M by neutrophils in rheumatoid arthritis

    Arthritis Rheum


  • J. Auer et al.

    Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis

    Arthritis Res Ther


  • T. Kasama et al.

    Expression of vascular endothelial growth factor by synovial fluid neutrophils in rheumatoid arthritis (RA)

    Clin Exp Immunol


  • G.S. Cheema et al.

    Elevated serum B lymphocyte stimulator levels in patients with systemic immune-based rheumatic diseases

    Arthritis Rheum


  • L.K. Assi et al.

    Tumor necrosis factor alpha activates release of B lymphocyte stimulator by neutrophils infiltrating the rheumatoid joint

    Arthritis Rheum


  • E.R. Vossenaar et al.

    Citrullination of synovial proteins in murine models of rheumatoid arthritis

    Arthritis Rheum


  • J.L. Eyles et al.

    Granulocyte colony-stimulating factor and neutrophils—forgotten mediators of inflammatory disease

    Nat Clin Pract Rheumatol


  • L. Bjorkman et al.

    Phagocyte-derived reactive oxygen species as suppressors of inflammatory disease

    Arthritis Rheum


  • J. Bylund et al.

    Enhanced inflammatory responses of chronic granulomatous disease leukocytes involve ROS-independent activation of NF-kappa B

    Eur J Immunol


  • Cited by (159)

    • The functional roles of m<sup>6</sup>A modification in T lymphocyte responses and autoimmune diseases

      2022, Cytokine and Growth Factor Reviews

      RNA N6-methyladenosine (m6A) modification is abundant in eukaryotes, bacteria and archaea. It is an RNA modification mainly existing in messenger RNA (mRNAs) and has a significant effect on the metabolism and function of mRNAs. m6A modification is controlled by three types of proteins, namely methyltransferase as the “writers”, demethylase as the “erasers”, and specific m6A recognized protein (YTHDF1–3) as the “readers”. Recent studies have shown that m6A modification plays an important role in cancer, viral infection and autoimmune diseases. In this review, we will elaborate on the m6A modifications in the homeostasis and differentiation of T cells. Then we will further summarize the effects of m6A modification on the T cell responses and T cell-mediated autoimmune diseases. This will advance T cell epigenetics research and provide potential biomarkers and therapeutic targets for autoimmune diseases.

    • An Integrated Pharmacological, Structural, and Genetic Analysis of Extracellular Versus Intracellular ROS Production in Neutrophils

      2022, Journal of Molecular Biology

      The neutrophil NADPH oxidase produces both intracellular and extracellular reactive oxygen species (ROS). Although oxidase activity is essential for microbial killing, and ROS can act as signaling molecules in the inflammatory process, excessive extracellular ROS directly contributes to inflammatory tissue damage, as well as to cancer progression and immune dysregulation in the tumor microenvironment. How specific signaling pathways contribute to ROS localization is unclear. Here we used a systems pharmacology approach to identify the specific Class I PI3-K isoform p110β, and PLD1, but not PLD2, as critical regulators of extracellular, but not intracellular ROS production in primary neutrophils. Combined crystallographic and molecular dynamics analysis of the PX domain of the oxidase component p47phox, which binds the lipid products of PI 3-K and PLD, was used to clarify the membrane-binding mechanism and guide the design of mutant mice whose p47phox is unable to bind 3-phosphorylated inositol phospholipids. Neutrophils from these K43A mutant animals were specifically deficient in extracellular, but not intracellular, ROS production, and showed increased dependency on signaling through the remaining PLD1 arm. These findings identify the PX domain of p47phox as a critical integrator of PLD1 and p110β signaling for extracellular ROS production, and as a potential therapeutic target for modulating tissue damage and extracellular signaling during inflammation.

    • Virtual Screening and In vitro Evaluation Identify Methotrexate and Testosterone are Inhibitors of Protein Arginine Deiminase 4

      2022, Archives of Medical Research

      Peptidyl arginine deiminases (PAD) are proteins that modify arginine residues to citrulline. In humans there are five isoforms PAD1-4 and PAD6. PAD4 is involved in several human diseases such as Alzheimer, breast cancer, rheumatoid arthritis and therefore has been recognized as a potential pharmacological target.

      In this work, 3175 molecules retrieved from ZINC12 Food and Drug Administration (FDA) catalog database were assayed through a structure-based virtual screening to identify potential PAD4 binders. Three were confirmed through enzyme inhibition studies. Flow cytometry analysis were used to check for drug cytotoxic effects on blood cells from three healthy donors.

      Molecular docking in a wild-type PAD4 structure showed the top 20 FDA molecules with the best binding energies. Those molecules were distributed in clusters of mixed binding energies but with similar chemical structures. These patterns along with the FDA information were used to aid in the rational selection of methotrexate, testosterone and leucovorin compounds for in vitro evaluations. Time course fluorescent enzyme kinetics confirmed that methotrexate (0.01–1 mmol) and testosterone enanthate (49.9–12.5 mmol) inhibit PAD4 at similar levels to the known inhibitor BB-Cl-amidine (8.8 mmol), except leucovorin. The chosen concentrations lack cytotoxic effects on blood cells.

      These findings encourage repositioning campaigns in the quest of PAD4 inhibitors.

      (Video) T Cell Effector Function: Part 2 - Th17 and T Regulatory Cells in Health and Disease
    • Rheumatoid arthritis: From synovium biology to cell-based therapy

      2022, Cytotherapy

      Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects the synovial joints and, if not treated properly, can lead to multiple progressive articular and extra-articular damage. Its pathogenesis is primarily associated with an inadequate immune response and dysregulated cytokine production. However, RA is also linked to disruption in oxygen metabolism, impaired redox signaling, acidosis and aberrant intercellular communication. Even though treatment modalities have made RA a manageable disease, a significant number of patients still do not respond satisfactorily or suffer considerably from the adverse events of conventional therapy. In recent years, cell-based strategies, especially the administration of the mesenchymal/medicinal stem/signaling cells (MSCs), have been proposed as a novel and very promising therapeutic approach. RA patients may benefit from the potent anti-inflammatory and immunomodulatory properties and tissue-repair potential of MSCs. Furthermore, the satisfactory safety profile of MSC therapy has been already demonstrated in several clinical studies. This review summarizes current understanding of the pathomechanism behind RA at the molecular and cellular level and focuses on MSC-based clinical research and applications of MSCs for RA treatment.

    • Innate immunity drives pathogenesis of rheumatoid arthritis

      2021, Biomedical Journal

      Rheumatoid arthritis (RA) is an autoimmune disease affecting ∼1% of the general population. This disease is characterized by persistent articular inflammation and joint damage driven by the proliferating synovial tissue fibroblasts as well as neutrophil, monocyte and lymphocyte trafficking into the synovium. The factors leading to RA pathogenesis remain poorly elucidated although genetic and environmental factors have been proposed to be the main contributors to RA. The majority of the early studies focused on the role of lymphocytes and adaptive immune responses in RA. However, in the past two decades, emerging studies showed that the innate immune system plays a critical role in the onset and progression of RA pathogenesis. Various innate immune cells including monocytes, macrophages and dendritic cells are involved in inflammatory responses seen in RA patients as well as in driving the activation of the adaptive immune system, which plays a major role in the later stages of the disease. Here we focus the discussion on the role of different innate immune cells and components in initiation and progression of RA. New therapeutic approaches targeting different inflammatory pathways and innate immune cells will be highlighted here. Recent emergence and the significant roles of innate lymphoid cells and inflammasomes will be also discussed.

    • Revision total elbow arthroplasty: Is it safe to perform a single-stage revision for presumed aseptic loosening based on clinical assessment, normal inflammatory markers, and a negative aspiration?

      2021, Journal of Shoulder and Elbow Surgery

      Revision total elbow arthroplasty (TEA) is a challenging procedure that is becoming increasingly common. In our unit, we regard it as essential to exclude infection as the underlying cause of TEA loosening. In all patients with arthroplasty loosening, we undertake a careful history and examination, perform radiographs, monitor inflammatory markers, and undertake a joint aspiration. If any investigation suggests infection as the etiology, then a 2-stage revision is undertaken. Open biopsies are not routinely performed. The aim was to ascertain from our outcomes whether it is safe to perform a single-stage revision for presumed aseptic loosening using these criteria.

      A retrospective review of a consecutive series of revision TEAs was performed in our unit over a 10-year period (2008-2018). Single-stage revisions performed for presumed aseptic loosening were identified. Case notes, radiographs, bloods, aspiration results, and microbiology of tissue samples taken at revision were reviewed.

      A total of 123 revision elbow arthroplasty cases were performed in the study period. Sixty cases were revised for preoperatively proven infection, instability, or implant failure and were excluded from this study. In 63 cases, aseptic loosening was diagnosed based on history, clinical examination, blood markers, and aspiration. There were 21 dual-component and 42 single-component revisions. In the dual-component revision group, tissue samples taken at the time of revision were positive in only 1 case (5%). In the single-component revision group, positive culture samples were present in 3 cases (7%). χ2analysis showed no significant difference between single- and dual-component revisions (P = .76). No cases with positive culture samples from either group have required subsequent revision surgery.

      Given the results of this study, we conclude that is safe to perform single-stage revision arthroplasty for implant loosening based on history, examination, normal inflammatory markers, and negative aspiration results without the need for open biopsy.

    View all citing articles on Scopus

    Recommended articles (6)

    • Research article

      Gender differences in circulating levels of neutrophil extracellular traps in serum of multiple sclerosis patients

      Journal of Neuroimmunology, Volume 261, Issues 1–2, 2013, pp. 108-119

      Neutrophil extracellular traps (NETs) trap and kill pathogens very efficiently but also activate dendritic cells and prime T cells. Previously, we demonstrated that neutrophils are primed and circulating NETs are elevated in relapsing remitting multiple sclerosis (RRMS), a T cell-mediated autoimmune disease. Here, we demonstrate gender specific differences in circulating NETs but not in neutrophil priming in RRMS patients. Although the results from our systematic and in depth characterization of these patients argue against a major role of circulating NETs in this disease, they suggest that NETs may underlie gender-specific differences in MS pathogenesis.

      (Video) Abbas 10: CD4 effector T cells (Raje)
    • Research article

      Possible involvement of elastase in enhanced osteoclast differentiation by neutrophils through degradation of osteoprotegerin

      Bone, Volume 132, 2020, Article 115216

      Neutrophils are one of the most abundant leukocytes in the sites of lesion of inflammatory diseases such as periodontitis and rheumatoid arthritis. These diseases are accompanied by bone loss, which worsens the quality of life of the patients. However, the role of neutrophils in the inflammatory bone loss has not been fully investigated. In the present study, we found that human neutrophils enhanced osteoclast differentiation from mouse bone marrow cells co-cultured with mouse osteoblasts in the presence of active vitamin D3. The enhanced osteoclast differentiation was significantly suppressed by elastatinal, a synthetic inhibitor of neutrophil elastase. Also, we found that human neutrophils degraded human recombinant osteoprotegerin (OPG), a decoy receptor for nuclear factor κB (RANK) ligand (RANKL), the essential osteoclast differentiation-inducing factor, expressed by osteoblasts. Degradation of OPG by neutrophils was suppressed by human α1-protease inhibitor, the major endogenous inhibitor of neutrophil elastase. Recombinant human neutrophil elastase degraded human OPG in its death domain-like region. These results indicated that the degradation of OPG by elastase contributed at least in part to the enhanced osteoclast differentiation by neutrophils. There is a possibility that neutrophils play an important role in inflammatory bone loss.

    • Research article

      Aging: A Temporal Dimension for Neutrophils

      Trends in Immunology, Volume 37, Issue 5, 2016, pp. 334-345

      Neutrophils are first-responders, providing early protection against invading pathogens. Recent findings have revealed a temporal dimension to neutrophil function, associated with the clearance cycles for aging neutrophils, and also with a program that endows circulating neutrophils with distinct phenotypic and functional properties at different times of the day, before they are cleared from blood. We review here the process of neutrophil aging and its impact on homeostasis and inflammation. We outline the features of aged neutrophils, examine proposed mechanisms that drive aging, and discuss how these processes may contribute to tissue homeostasis and pathology. In this context we propose that neutrophil aging may optimize host defense by allowing neutrophils to anticipate infections while avoiding permanent activation and subsequent damage.

    • Research article

      Eosinophils are dispensable for development of MOG35–55-induced experimental autoimmune encephalomyelitis in mice

      Immunology Letters, Volume 239, 2021, pp. 72-76

      Experimental autoimmune encephalomyelitis (EAE) represents the mouse model of multiple sclerosis, a devastating neurological disorder. EAE development and progression involves the infiltration of different immune cells into the brain and spinal cord. However, less is known about a potential role of eosinophil granulocytes for EAE disease pathogenesis. In the present study, we found enhanced eosinophil abundance accompanied by increased concentration of the eosinophil chemoattractant eotaxin-1 in the spinal cord in the course of EAE induced in C57BL/6 mice by immunization with MOG35–55 peptide. However, the absence of eosinophils did not affect neuroinflammation, demyelination and clinical development or severity of EAE, as assessed in ∆dblGATA1 eosinophil-deficient mice. Taken together, despite their enhanced abundance in the inflamed spinal cord during disease progression, eosinophils were dispensable for EAE development.

    • Research article

      Metabolic signatures of T-cells and macrophages in rheumatoid arthritis

      Current Opinion in Immunology, Volume 46, 2017, pp. 112-120

      In most autoimmune diseases, a decade-long defect in self-tolerance eventually leads to clinically relevant, tissue-destructive inflammatory disease. The pathogenic potential of chronic persistent immune responses during the pre-clinical and clinical phase is ultimately linked to the bioenergetic fitness of innate and adaptive immune cells. Chronic immune cell stimulation, high cellular turn-over, structural damage to the host tissue and maladaptive wound healing, all require a reliable supply of nutrients, oxygen, and biosynthetic precursors. Here, we use the model system of rheumatoid arthritis (RA) to discuss immunometabolism from the vantage point of T-cells and macrophages that encounter fundamentally different metabolic stress scenarios in the RA host. We outline the general principle that both insufficient nutrient supply, as well as nutrient excess generate cellular stress responses and guide immune function. ATPlow, NADPHhigh, ROSlow T-cells hyperproliferate and are forced into premature senescence. ATPhigh, ROShigh macrophages dimerize the glycolytic enzyme pyruvate kinase to amplify STAT3-dependent inflammatory effector functions. A corollary of this model is that simple nutraceutical interventions will be insufficient to re-educate the immune system in RA. Instead, interference with cell-type-exclusive and differentiation-stage-dependent metabolic setpoints will be needed to reprogram arthritogenic pathways.

    • Research article

      The role of neutrophils in host defense and disease

      Journal of Allergy and Clinical Immunology, Volume 145, Issue 6, 2020, pp. 1535-1544

      Neutrophils, the most abundant circulating leukocyte, are critical for host defense. Granulopoiesis is under the control of transcriptional factors and culminates in mature neutrophils with a broad armamentarium of antimicrobial pathways. These pathways include nicotinamide adenine dinucleotide phosphate oxidase, which generates microbicidal reactive oxidants, and nonoxidant pathways that target microbes through several mechanisms. Activated neutrophils can cause or worsen tissue injury, underscoring the need for calibration of activation and resolution of inflammation when infection has been cleared. Acquired neutrophil disorders are typically caused by cytotoxic chemotherapy or immunosuppressive agents. Primary neutrophil disorders typically result from disabling mutations of individual genes that result in impaired neutrophil number or function, and provide insight into basic mechanisms of neutrophil biology. Neutrophils can also be activated by noninfectious causes, including trauma and cellular injury, and can have off-target effects in which pathways that typically defend against infection exacerbate injury and disease. These off-target effects include acute organ injury, autoimmunity, and variable effects on the tumor microenvironment that can limit or worsen tumor progression. Agreater understanding of neutrophil plasticity in these conditions is likely to pave the way to new therapeutic approaches.

      (Video) 2015 T Cell Effector Function (TH1, TH2, TH17) and Cytokine Biology
    View full text

    Copyright © 2010 Elsevier B.V. All rights reserved.


    What do neutrophils do in rheumatoid arthritis? ›

    Neutrophils regulate immune and inflammatory response in RA

    Besides secreting proteases, activated neutrophils act like macrophages or dendritic cells in the regulation of adaptive immune response.

    Can rheumatoid arthritis cause high neutrophils? ›

    The association between NLR and disease activity was analyzed. Results: Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and neutrophil counts were significantly higher in RA and AS patients compared to healthy controls.

    Can rheumatoid arthritis cause low neutrophils? ›

    Felty's syndrome is a rare complication of RA, first described in 1924. Its features are low neutrophils (white blood cells) in the blood, infections and leg ulcers in a patient who usually has severe RA.

    Can high neutrophils mean arthritis? ›

    Rheumatoid arthritis. The identification of increased neutrophils in RA synovial fluid, particularly in early disease stages, supports a role for these cells in the pathogenesis of joint destruction [81–85].

    What does it mean if neutrophils are high? ›

    Having a high percentage of neutrophils in your blood is called neutrophilia. This is a sign that your body has an infection. Neutrophilia can point to a number of underlying conditions and factors, including: infection, most likely bacterial.

    What do neutrophils release during inflammation? ›

    Neutrophils respond to multiple signals and respond by producing several cytokines and other inflammatory factors that influence and regulate inflammation and also the immune system (Nauseef and Borregaard, 2014; Scapini and Cassatella, 2014).

    How does RA cause neutropenia? ›

    Autoimmunity with the production of antibodies against granulocytes can cause neutropenia [12]. In patients with RA, the autoimmune process is usually related either to the RA itself or to concomitant Sjögren's syndrome [12], [13].

    What does it mean when neutrophils are low? ›

    Neutropenia is a blood condition characterized by low levels of neutrophils, which are white blood cells that protect your body from infections. Without enough neutrophils, your body can't fight off bacteria. Having neutropenia increases your risk for many types of infection.

    What can cause low neutrophils? ›

    What causes a low neutrophil count? Neutropenia is the result of your body destroying neutrophils before your bone marrow can create more. Causes of a low neutrophil count include: Infection (hepatitis, tuberculosis, sepsis, Lyme disease).

    What does elevated WBC and neutrophils mean? ›

    Neutrophils are a type of white blood cell. They help you fight infection. If there are too many neutrophils in your bloodstream, you may develop leukocytosis, or a high total white blood cell count. You may have symptoms such as fevers or recurring infections. These symptoms may be signs of an underlying condition.


    1. Immunology of the rheumatoid joint
    (nature video)
    2. Rewriting the etiology and pathogenesis of rheumatoid arthritis?
    3. Pre-Rheumatoid Arthritis: Can We Define It and Prevent Its Progression?
    4. UW Rheumatology Grand Rounds - Dr. John Isaacs, 11/16/2021
    (Rheum Washington)
    5. Pauci-immune Glomerulonephritis: Overview and Updates
    (Glomerular Disease Study & Trial Consortium)
    6. Abbas 10: Differentiation and Function of CD4+ Effector Cells (Raje)

    You might also like

    Latest Posts

    Article information

    Author: Lidia Grady

    Last Updated: 06/08/2022

    Views: 6235

    Rating: 4.4 / 5 (65 voted)

    Reviews: 88% of readers found this page helpful

    Author information

    Name: Lidia Grady

    Birthday: 1992-01-22

    Address: Suite 493 356 Dale Fall, New Wanda, RI 52485

    Phone: +29914464387516

    Job: Customer Engineer

    Hobby: Cryptography, Writing, Dowsing, Stand-up comedy, Calligraphy, Web surfing, Ghost hunting

    Introduction: My name is Lidia Grady, I am a thankful, fine, glamorous, lucky, lively, pleasant, shiny person who loves writing and wants to share my knowledge and understanding with you.