Autoimmune Phenomena Research Articles

The Role of Molecular Chaperones in Virus Infection and Implications for Understanding and Treating COVID-19.

The COVID-19 pandemic made imperative the search for means to end it, which requires a knowledge of the mechanisms underpinning the multiplication and spread of its cause, the coronavirus SARS-CoV-2. Many viruses use members of the hosts’ chaperoning system to infect the target cells, replicate, and spread, and here we present illustrative examples. Unfortunately, the role of chaperones in the SARS-CoV-2 cycle is still poorly understood. In this review, we examine the interactions of various coronaviruses during their infectious cycle with chaperones in search of information useful for future research on SARS-CoV-2. We also call attention to the possible role of molecular mimicry in the development of autoimmunity and its widespread pathogenic impact in COVID-19 patients. Viral proteins share highly antigenic epitopes with human chaperones, eliciting anti-viral antibodies that crossreact with the chaperones. Both, the critical functions of chaperones in the infectious cycle of viruses and the possible role of these molecules in COVID-19 autoimmune phenomena, make clear that molecular chaperones are promising candidates for the development of antiviral strategies. These could consist of inhibiting-blocking those chaperones that are necessary for the infectious viral cycle, or those that act as autoantigens in the autoimmune reactions causing generalized destructive effects on human tissues.

Autoimmune phenomena involving the pituitary gland in children: New developing data about diagnosis and treatment

Autoimmune phenomena involving the pituitary gland in children: New developing data about diagnosis and treatment

The triggering of post-COVID-19 autoimmunity phenomena could be associated with both transient immunosuppression and an inappropriate form of immune reconstitution in susceptible individuals

With the progression of the COVID-19 pandemic, there have been different reports about the development of autoimmune diseases once the infection is controlled. After entering the respiratory epithelial cells, SARS-CoV-2—the virus that causes the disease—triggers a severe inflammatory state in some patients known as “cytokine storm” and the development of thrombotic phenomena—both conditions being associated with high mortality. Patients additionally present severe lymphopenia and, in some cases, complement consumption and autoantibody development. There is a normalization of lymphocytes once the infection is controlled. After this, autoimmune conditions of unknown etiology may occur. A hypothesis for the development of post-COVID-19 autoimmunity is proposed based on the consequences of both a transient immunosuppression (both of innate and acquired immunity) in which self-tolerance is lost and an inappropriate form of immune reconstitution that amplifies the process.

Ground Zero Revisited – Museums and Materiality in an Age of Global Pandemic

This paper examines the potential of convergence technologies in the process of 9/11 memorialization, particularly when materiality and its absence are so crucial to the in-situ narrative of post terror attack. Questions over the incorporation of virtual and digital media are not new in the context of COVID-19 but are perhaps more urgent than ever, as we all begin to grapple with the turn to technology as a surrogate for what we cannot physically provide. In particular, I trace the Derridean phenomenon of autoimmunity to draw parallels between memorial practices associated with both 9/11 and COVID-19. Ultimately, the migration online initiated by global pandemic reminds us that traumatic memory in particular is punctuated by gaps and absences; it insists on the recognition of other, stranger, incomplete and imperfect ways of knowing and commemorating.

COVID-19: A Great Mime or a Trigger Event of Autoimmune Manifestations?

Viruses can induce autoimmune diseases, in addition to genetic predisposition and environmental factors. Particularly, coronaviruses are mentioned among the viruses implicated in autoimmunity. Today, the world's greatest threat derives from the pandemic of a new human coronavirus, called "severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the responsible agent of coronavirus disease 2019 (COVID-19). First case of COVID-19 was identified in Wuhan, the capital of Hubei, China, in December 2019 and quickly spread around the world. This review focuses on autoimmune manifestations described during COVID-19, including pro-thrombotic state associated with antiphospholipid antibodies (aPL), acute interstitial pneumonia, macrophage activation syndrome, lymphocytopenia, systemic vasculitis, and autoimmune skin lesions. This offers the opportunity to highlight the pathogenetic mechanisms common to COVID-19 and several autoimmune diseases in order to identify new therapeutic targets. In a supposed preliminary pathogenetic model, SARS-CoV-2 plays a direct role in triggering widespread microthrombosis and microvascular inflammation, because it is able to induce transient aPL, endothelial damage and complement activation at the same time. Hence, endothelium might represent the common pathway in which autoimmunity and infection converge. In addition, autoimmune phenomena in COVID-19 can be explained by regulatory T cells impairment and cytokines cascade.

Acute liver failure-The importance of rapid diagnostics and early initiation of treatment

Acute liver failure (ALF) is a rare disease with high mortality. It is defined as coagulopathy and encephalopathy in a person with a previously healthy liver. The etiology of ALF is a decisive prognostic factor and varies depending on the country of origin of the patient. Although in many countries the main triggers are hepatotropic viruses, in western industrial countries toxic medicinal causes and autoimmune phenomena predominate. The course of ALF runs through various phases. The complete picture of ALF can mostly no longer be casually treated but necessitates in particular timely contact with a transplantation center. If a causal treatment exists, the effectiveness is greatly dependent on the timing of initiation. In the best case scenario this can completely avoid liver damage. In the complete picture of ALF the main focus is on the intensive medical care of a threatening multiorgan failure. In this context new standards of treatment were established by studies on plasmapheresis.

S1584 Autoimmune Exocrine Pancreatic Insufficiency: A Novel Paraneoplastic Mechanism for Diarrhea in Patients With Thymoma

INTRODUCTION: Paraneoplastic syndromes are an exceedingly rare cause of chronic diarrhea. Thymomas have been associated with two known paraneoplastic diarrheal syndromes, namely in the context of hypogammaglobulinemia (Good’s syndrome) or a graft-versus-host disease (GVHD)-like condition. However, exocrine pancreatic insufficiency has yet to be reported as a cause of diarrhea in patients with thymoma. CASE DESCRIPTION/METHODS: A 36-year-old woman with no known medical morbidities presented with postprandial watery diarrhea, emesis, and 100-lb unintentional weight loss over two years. Labs were notable for lymphocytosis up to 8,100/mL with normal flow cytometry and no abnormalities on blood smear. Celiac disease serologies and stool infectious studies were negative. Immunoglobulin G levels were elevated at 3,010 mg/dL, and stool pancreatic elastase levels were low (< 15 mg/g). Additional labs were consistent with fat soluble vitamin deficiency: vitamin A < 5 mcg/dL, 25-hydroxyvitamin D < 4 ng/dL, vitamin E 7 mg/L, vitamin K 69 pg/mL. Computed tomography (CT) of the chest revealed an 11-cm anterior mediastinal mass with pleural and nodal metastases, and biopsy was suggestive of malignant thymoma (Figure 1). CT of the abdomen revealed a normal-appearing pancreas. Subsequent endoscopy and colonoscopy showed healthy-appearing mucosa with no abnormalities (Figure 2). However, colonic biopsies were notable for mild diffuse inflammatory changes including scattered intraepithelial lymphocytes and neutrophils, increased apoptotic bodies, and crypt architectural distortion. Her diarrhea ultimately improved after four cycles of induction chemotherapy. DISCUSSION: GVHD-like colitis in patients with malignant thymoma has been reported in several instances. This has been attributed to alterations in the thymic microenvironment, which lead to dysregulation and loss of anergy. Autoreactive T-cells can mount an immune response that impacts a number of organs, especially in the gastrointestinal tract. Although our patient had histopathological changes reflective of colitis secondary to GVHD, the severity of her diarrhea was out-of-proportion to these findings. The postprandial nature of her symptoms and markedly low stool pancreatic elastase were suggestive of possible pancreatic insufficiency, likely secondary to an autoimmune phenomenon impacting the exocrine glands of the pancreas. This case proposes a possible novel paraneoplastic mechanism for diarrhea in patients with thymoma.Figure 1.: Cross-section image of anterior mediastinal mass.Figure 2.: Normal-appearing duodenal mucosa.

Lens and Intraocular Lens-Induced Uveitis; Clinic, Diagnosis, and Treatment

Lens-induced uveitis is a rare form of uveitis. It is an autoimmune phenomenon secondary to lens proteins that go out of the lens capsule due to exogenous or iatrogenic (surgical) trauma. The classic history and eye examination findings are typical for diagnosis. For the treatment, surgery is usually chosen in the forefront. Intraocular lens-induced uveitis is a rare form of uveitis that can be seen as a result of micro-and macro trauma of intraocular lens implants to intraocular tissues (iris, ciliary body, iridocorneal angle, etc.). Although this entity can be regressed by medical treatment, the definitive treatment is the removal or repositioning of the intraocular lens according to the etiological event. With the development of minimal traumatic surgical techniques and the use of new intraocular lens implants, its frequency decreases. The aim of this review is to summarize the general features, diagnosis, and treatment of uveitis due to lenses and intraocular lenses.

Drug-Induced Lupus Erythematosus Associated with Proton Pump Inhibitor

AbstractDrug-induced lupus erythematosus is an autoimmune phenomenon where the drug exposure leads to the development of systemic lupus erythematous like clinical features. Drug-induced lupus erythematosus can be divided into systemic lupus erythematous, subacute cutaneous lupus erythematous, and chronic cutaneous lupus erythematous. Here, we report a case of a 29-year-old female presented with systemic lupus erythematous due to chronic use of proton pump inhibitors, which is considered to be very rare.

Immunogenicity, Tolerability, and Clinical Effectiveness of 23-Valent Polysaccharide Pneumococcal Vaccine in Patients with Systemic Lupus Erythematosus

The aim of the work is to study the immunogenicity, tolerability, and clinical efficacy of the 23-valent polysaccharide pneumococcal vaccine (PPV-23) in patients with systemic lupus erythematosus (SLE). Material and methods. The study included 61 patients with a confirmed diagnosis of SLE, including 53 women, 8 men, aged 19 to 68 years. The disease activity at the time of vaccination: in 9 patients — high, in 13 — medium, in 34 — low, in 5 — remission. Therapy outline: 59 patients received glucocorticoids (GC) 5–30 mg/day in terms of prednisolone, 45 — hydroxychloroquine (GC), 33 — cytostatics (CS), 22 — genetically engineered biological drugs (GEBD): 11 — rituximab (RTM), 10 — belimumab (BLM). 23-valent polysaccharide pneumococcal vaccine in an amount of 0.5 ml (1 dose) was injected subcutaneously. Follow-up period: 9 patients — 3 months, 52 — 1 year after the vaccination. Patients were examined before vaccination, as well as in 1, 3, and 12 months after the vaccination. Results and discussion. After a year of observation, the number of «responders» to vaccination was 61.5%, «non-responders» — 38.5%. There was a decreased response to vaccine in patients receiving GEBD compared with patients who did not receive GEBD (40% and 75%, respectively), p=0.02. No differences were found against the background of RTM and BLM therapy. Administering GC in a dose exceeding 10 mg/day did not lead to a more significant decrease in response to vaccine compared to other patients. Standard local vaccination reactions of mild to moderate severity were noted in 50.8% of the patients, general reaction of mild severity — in 1 patient (1.6%), hyperergic Arthus-like reaction — in 1 patient (1.6%), the symptoms of which were relieved in 7 days. During the observation period (1 year), not a single case of exacerbation of SLE, reliably associated with the vaccination, was registered, and no new autoimmune phenomena were identified. Clinically positive dynamics was noted in the form of a decrease in the number of episodes of pneumonia, as well as acute and exacerbated chronic bronchitis, sinusitis. Conclusion. Sufficient immunogenicity, good tolerance, and clinical effectiveness of PPV-23 in patients with SLE, incl. those, who received combined immunosuppressive therapy. Further studies are needed in large groups of patients with long follow-up periods.

Basic immunology may lead to translational therapeutic rationale: SARS-CoV-2 and rheumatic diseases.

COVID‐19 pandemia is a major concern for patients and healthcare systems. The fear of infection by patients with concomitant rheumatic diseases (either adult or children) and connective tissue diseases is arising worldwide, because of their immunological background and immunological therapies. Analysing the basic biology of single diseases, the data suggest that there is an "immunological umbrella" that seems to protect against the infection, through IFN type 1 and NK cell function. To date, reports from China, United States and Europe did not reveal an higher risk of infection, either for rheumatoid arthritis, juvenile idiopathic arthritis nor for lupus erythematosus. Antimalarials, anti‐IL6‐Anti‐IL6 receptor, anti‐IL1, anti‐GM‐CSF receptor and JAK1/2/3 inhibitors, are under investigation in COVID‐dedicated clinical trials to control the inflammation raised by SARS‐CoV‐2 infection. Initial reports on the occurrence of autoimmune phenomena in the convalescence phase of SARS‐CoV‐2 infection suggests that the immunological consequences of the infection need to be strictly understood. Reporting of the study conforms to broad EQUATOR guidelines (Simera et al January 2010 issue of EJCI).

Metabolic optimization of adoptive T cell transfer cancer immunotherapy: A historical overview.

After prolonged extracorporeal multiplication in physiological culture media, there can be curative infusions of a cancer patient's own cytotoxic T cells (adoptive T cell transfer; ACT), which must achieve efficient activation in potentially adverse tumour microenvironments. With spectacular, yet irregular, success, improvements are needed. Developing lymphoid cells are biologically selected, not only for 'near-self' reactivity (positive selection), but also to avoid self-reactivity (negative selection). Thus, success requires harnessing near-self cells while avoiding extreme autoimmune phenomena. Abrupt metabolic changes accompanying T cell activation to leave the G0 stage and enter the G1 stage of the cell cycle (eg enhanced glycolysis) are accompanied by increased transcription of the G0S9 gene that mediates salvage synthesis of NAD+ from nicotinamide; the latter has recently been shown to increase the efficiency of ACT. Despite theoretical and experimental advances, there has not been parallel progress in simulating in vivo conditions with culture media that were initially formulated for their positive benefits for tumour cell lines (cell survival and proliferation). Yet for lymphoid cells, inhibition or death (ie immunological tolerance) is as important as their activation and proliferation (immunological response). Thus, use of media optimized for the latter may mask the former. The resilience of established culture protocols may have been partly politically driven. However, unphysiological conditions have sometimes yielded fortuitous insights. Optimization of culture media for specific tissues must consider the nature of problems addressed in research settings and the need to avoid mishaps in clinical settings.

S-adenosyl-L-methionine (SAMe) halts the autoimmune response in patients with primary biliary cholangitis (PBC) via antioxidant and S-glutathionylation processes in cholangiocytes

S-adenosyl-L-methionine is an endogenous molecule with hepato-protective properties linked to redox regulation and methylation. Here, the potential therapeutic value of SAMe was tested in 17 patients with PBC, a cholestatic disease with autoimmune phenomena targeting small bile ducts. Nine patients responded to SAMe (SAMe responders) with increased serum protein S-glutathionylation. That posttranslational protein modification was associated with reduction of serum anti-mitochondrial autoantibodies (AMA-M2) titers and improvement of liver biochemistry. Clinically, SAMe responders were younger at diagnosis, had longer duration of the disease and lower level of serum S-glutathionylated proteins at entry. SAMe treatment was associated with negative correlation between protein S-glutathionylation and TNFα. Furthermore, AMA-M2 titers correlated positively with INFγ and FGF-19 while negatively with TGFβ. Additionally, cirrhotic PBC livers showed reduced levels of glutathionylated proteins, glutaredoxine-1 (Grx-1) and GSH synthase (GS). The effect of SAMe was also analyzed in vitro. In human cholangiocytes overexpressing miR-506, which induces PBC-like features, SAMe increased total protein S-glutathionylation and the level of γ-glutamylcysteine ligase (GCLC), whereas reduced Grx-1 level. Moreover, SAMe protected primary human cholangiocytes against mitochondrial oxidative stress induced by tBHQ (tert-Butylhydroquinone) via raising the level of Nrf2 and HO-1. Finally, SAMe reduced apoptosis (cleaved-caspase3) and PDC-E2 (antigen responsible of the AMA-M2) induced experimentally by glycochenodeoxycholic acid (GCDC). These data suggest that SAMe may inhibit autoimmune events in patients with PBC via its antioxidant and S-glutathionylation properties. These findings provide new insights into the molecular events promoting progression of PBC and suggest potential therapeutic application of SAMe in PBC.

Phenotype variability of autoinflammatory disorders in the pediatric patient: A pictorial overview.

Disruption of innate immunity leading to systemic inflammation and multi-organ dysfunction is the basilar footprint of autoinflammatory disorders (AIDs), ranging from rare hereditary monogenic diseases to a large number of common chronic inflammatory conditions in which there is a simultaneous participation of multiple genetic components and environmental factors, sometimes combined with autoimmune phenomena and immunodeficiency. Whatever their molecular mechanism, hereditary AIDs are caused by mutations in regulatory molecules or sensors proteins leading to dysregulated production of proinflammatory cytokines or cytokine-inducing transcription factors, fever, elevation of acute phase reactants, and a portfolio of manifold inflammatory signs which might occur in a stereotyped manner, mostly with overactivity or misactivation of different inflammasomes. Symptoms might overlap in the pediatric patient, obscuring the final diagnosis of AIDs and delaying the most appropriate treatment. Actually, the fast-paced evolution of scientific knowledge has led to recognize or reclassify an overgrowing number of multifactorial diseases, which share the basic pathogenetic mechanisms with AIDs. The wide framework of classic hereditary periodic fevers, AIDs with prominent skin involvement, disorders of the ubiquitin-proteasome system, defects of actin cytoskeleton dynamics, and also idiopathic nonhereditary febrile syndromes occurring in children is herein presented. Interleukin-1 dependence of these diseases or involvement of other predominating molecules is also discussed.

Does SARS-CoV-2 Trigger Stress-InducedAutoimmunity by Molecular Mimicry? A Hypothesis.

Viruses can generate molecular mimicry phenomena within their hosts. Why should severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not be considered one of these? Information in this short review suggests that it might be so and, thus, encourages research aiming at testing this possibility. We propose, as a working hypothesis, that the virus induces antibodies and that some of them crossreact with host’s antigens, thus eliciting autoimmune phenomena with devasting consequences in various tissues and organs. If confirmed, by in vitro and in vivo tests, this could drive researchers to find effective treatments against the virus.

The localization of HPV and CMV in the adipose tissues of female diabetic type 1 rats and the possibility of having a role of reactivity of COVID-19 in diabetic subjects as a new medical hypothesis

Introduction: Diabetes has various impacts on human body. It is thought that diabetes is predisposed by obesity. Obesity may due to several factors including genetically-environmental factors. The recent views that viruses may act as etiology for obesity. Study objectives: The main objectives of the present study were to investigate the possibility that CMV and HPV of having a role in initiating episodes of obesity and diabetes, and to test the hypothesis that co-existence of multi-viruses including corona virus may work synergistically to increase the impact of COVID-19 on diabetic patients. Methodology: In this study, a diabetic model was induced, the localization of HPV and CMV was determined using immunohistochemistry. Results: Study findings showed that both viruses HPV and CMV exist in the adipose tissue of diabetic rats. Both viruses were brown in color. Conclusions: Taken together, both CMV and HPV exist in the adipose tissue of diabetic rats, and this may explain the phenomenon of autoimmunity in diabetes from one side and from another side, we may explain the occurrence of synergistic effects of COVID-19 virus and the other viruses mentioned in this study.

Side effect management during immune checkpoint blockade using CTLA-4 and PD-1 antibodies for metastatic melanoma - an update.

CTLA-4 and PD-1 play a key role in tumor-induced downregulation of lymphocytic immune responses. Immune checkpoint inhibitors have been shown to alter the immune response to various cancer types. Anti-CTLA-4 and anti-PD-1 antibodies affect the interaction between tumor, antigen-presenting cells and Tlymphocytes. Clinical studies of the anti-CTLA-4 antibody ipilimumab and the anti-PD-1 antibodies nivolumab and pembrolizumab have provided evidence of their positive effects on overall survival in melanoma patients. Combined treatment using ipilimumab and nivolumab has been shown to achieve five-year survival rates of 52%. Such enhancement of the immune response is inevitably associated with adverse events. Knowledge of the spectrum of side effects is essential, both in terms of prevention and management. Adverse events include colitis, dermatitis, hypophysitis, thyroiditis, hepatitis and other, less common autoimmune phenomena. In recent years, considerable progress has been made in the detection and treatment of the aforementioned immune-related adverse events. However, early diagnosis of rare neurological or cardiac side effects, which may be associated with increased mortality, frequently pose a challenge. The present update highlights our current understanding as well as new insights into the spectrum of side effects associated with checkpoint inhibitors and their management.

Intestinal Anti-tissue Transglutaminase2 Autoantibodies: Pathogenic and Clinical Implications for Celiac Disease.

Celiac disease (CD) is a systemic disease that primarily affects the small intestine. The presence of anti-tissue transglutaminase 2 (anti-TG2) antibodies in the serum, as well as the presence of autoimmune phenomena, account for the inclusion of CD among autoimmune diseases. Anti-TG2 autoantibodies are produced at intestinal level, where they are deposited even before they appear in circulation. The pathogenic events that lead to their production are still not completely defined, but a central role seems to be played by gliadin-specific T cells. Interestingly, limited somatic mutations have been observed in VH and VL genes in TG2-specific plasma cells, another important aspect being the biased use of a heavy chain encoded by the VH5 gene. Conflicting data have been produced over the years on the effect of anti-TG2 antibodies on TG2 function. Although the presence of anti-TG2 antibodies in serum is considered a hallmark of CD and relevant from a clinical viewpoint, the role of these autoantibodies in the development of the celiac lesion remains to be defined. In the years, different technical approaches have been implemented to detect and measure intestinal CD-associated autoantibody production. Two aspects can make intestinal anti-TG2 antibodies relevant: from a clinical viewpoint: the first is their proposed ability in potential coeliac patients to predict the development of a full-blown enteropathy; the second is their possible role in revealing a condition of reactivity to gluten in patients with no circulating CD-associated autoantibodies. In fact, the detection of CD-specific autoantibodies production in the intestine, in the absence of serum positivity for the same antibodies, could be suggestive of a very early condition of gluten reactivity; alternatively, it could be not specific for CD and merely attributable to intestinal inflammation. In conclusion, the role of mucosal anti-TG2 antibodies in pathogenesis of CD is unknown. Their presence, the modalities of their production, their gluten dependence render them a unique model to study autoimmunity.

Suboptimal treatment response to anti-IL-5 monoclonal antibodies in severe eosinophilic asthmatics with airway autoimmune phenomena.

In clinical trials, the two anti-interleukin (IL)-5 monoclonal antibodies (mAbs: mepolizumab and reslizumab) approved to treat severe eosinophilic asthma reduce exacerbations by ∼50-60%. To observe response to anti-IL-5 mAbs in a real-life clinical setting, and to evaluate predictors of suboptimal response. In four Canadian academic centres, predefined clinical end-points in 250 carefully characterised moderate-to-severe asthmatic patients were collected prospectively to assess response to the two anti-IL-5 mAbs. Suboptimal response was determined based on failure to reduce maintenance corticosteroid (MCS) or asthma symptoms scores (Asthma Control Questionnaire (ACQ)) or exacerbations, in addition to persistence of sputum/blood eosinophils. Worsening in suboptimal responders was assessed based on reduced lung function by 25% or increase in MCS/ACQ. A representative subset of 39 patients was evaluated for inflammatory mediators, autoantibodies and complement activation in sputum (by ELISA) and for immune-complex deposition by immunostaining formalin-fixed paraffin-embedded sputum plugs. Suboptimal responses were observed in 42.8% (107 out of 250) patients treated with either mepolizumab or reslizumab. Daily prednisone requirement, sinus disease and late-onset asthma diagnoses were the strongest predictors of suboptimal response. Asthma worsened in 13.6% (34 out of 250) of these patients. The majority (79%) of them were prednisone-dependent. Presence of sputum anti-eosinophil peroxidase immunoglobulin (Ig)G was a predictor of suboptimal response to an anti-IL-5 mAb. An increase in sputum C3c (marker of complement activation) and deposition of C1q-bound/IL-5-bound IgG were observed in the sputa of those patients who worsened on therapy, suggesting an underlying autoimmune-mediated pathology. A significant number of patients who meet currently approved indications for anti-IL5 mAbs show suboptimal response to them in real-life clinical practice, particularly if they are on high doses of prednisone. Monitoring blood eosinophil count is not helpful to identify these patients. The concern of worsening of symptoms associated with immune-complex mediated complement activation in a small proportion of these patients highlights the relevance of recognising airway autoimmune phenomena and this requires further evaluation.

Clinical and Autoimmune Characteristics of Severe and Critical Cases of COVID-19.

In this study we report on the clinical and autoimmune characteristics of severe and critical novel coronavirus pneumonia caused by severe acute respiratory syndrome‒associated coronavirus 2 (SARS‐CoV‐2). The clinical, autoimmune, and laboratory characteristics of 21 patients who had laboratory‐confirmed severe and critical cases of coronavirus disease 2019 (COVID‐19) from the intensive care unit of the Huangshi Central Hospital, Hubei Province, China, were investigated. A total of 21 patients (13 men and 8 women), including 8 (38.1%) severe cases and 13 (61.9%) critical cases, were enrolled. Cough (90.5%) and fever (81.0%) were the dominant symptoms, and most patients (76.2%) had at least one coexisting disorder on admission. The most common characteristics on chest computed tomography were ground‐glass opacity (100%) and bilateral patchy shadowing (76.2%). The most common findings on laboratory measurement were lymphocytopenia (85.7%) and elevated levels of C‐reactive protein (94.7%) and interleukin‐6 (89.5%). The prevalence of anti‒52 kDa SSA/Ro antibody, anti‒60 kDa SSA/Ro antibody, and antinuclear antibody was 20%, 25%, and 50%, respectively. We also retrospectively analyzed the clinical and laboratory data from 21 severe and critical cases of COVID‐19. Autoimmune phenomena exist in COVID‐19 subjects, and the present results provide the rationale for a strategy of preventing immune dysfunction and optimal immunosuppressive therapy.