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. 2025 Jan 3;39(1):539–547. doi: 10.21873/invivo.13858

Precision Assessment of Anti-NMDA Receptor Encephalitis: A Case Report on Integrating Clinical Course, Immunophenotyping, and Comprehensive Symptomatology in a Pediatric Patient With Adjunctive Hydrogen Therapy

SHANG-CHIANG LIN 1, JENG-WEI LU 2,3, TING-CHUN LIN 4, YUEH-FENG SUNG 5, YI-JUNG HO 4,6, FU-MIN WANG 7, SHAN-WEN LUI 8, TING-YU HSIEH 8, KUANG-YIH WANG 9, FENG-CHENG LIU 9
PMCID: PMC11705097  PMID: 39740868

Abstract

Background/Aim

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, though rare, is the most common form of autoimmune encephalitis, predominantly affecting young individuals, particularly females. Standard treatments include corticosteroids, intravenous immunoglobulins (IVIG), and plasmapheresis, with rituximab recommended for those unresponsive to first-line therapies. However, reliable biomarkers for clinical assessment remain elusive. This study investigated the efficacy of adjunctive hydrogen therapy in a patient with anti-NMDAR encephalitis.

Case Report

This case report describes a 14-year-old boy with anti-NMDAR encephalitis who exhibited poor response to initial treatment, but showed significant improvement with rituximab and adjunctive hydrogen therapy. Immunophenotyping revealed correlations between treatment outcomes and shifts in B cell subsets, PD-1+ cytotoxic T cells, and regulatory T cell subtypes.

Conclusion

This case underscores the importance of integration traditional clinical assessments with advanced diagnostics such as flow cytometry-based immunophenotyping, and suggests a potential role for hydrogen therapy in modulating immune response in this complex autoimmune condition.

Keywords: Case report, anti-NMDA receptor encephalitis, B cells, PD-1+ cytotoxic T cells, regulatory T cells, hydrogen therapy

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a rare autoimmune disorder of the central nervous system, characterized by the presence immunoglobulin G (IgG) antibodies targeting NMDA receptors. Although classified as a rare disease, with an incidence estimated at 1 in 1.5 million people per year, anti-NMDAR encephalitis is the most common form of antibody-mediated encephalitis. It predominantly affects young adults and children, particularly females, often in association with ovarian teratomas (1,2). Clinical symptoms of anti-NMDAR encephalitis may appear similar across patients several weeks (3-4 weeks) after onset; however, significant differences can emerge between children and adults within the first few days to two weeks (3). Children often present with neurological symptoms, such as movement disorders or seizures, whereas adults more commonly exhibit psychiatric symptoms, including depression, mania, and visual or auditory hallucination. Additionally, patients with anti-NMDAR encephalitis can experience both positive and negative psychiatric symptoms (1,3). Although these psychiatric symptoms may resemble primary psychiatric disorders, their onset in anti-NMDAR encephalitis is typically more rapid (1-3). The clinical manifestations of anti-NMDAR encephalitis can worsen progressively over days to weeks.

Despite the challenges in diagnosing and managing anti-NMDAR encephalitis, experts have established clear established diagnostic criteria and treatment guidelines. A diagnosis of anti-NMDAR encephalitis can be made in patients who test positive for NMDAR antibodies in cerebrospinal fluid (CSF) and/or serum, combined with the presence of psychiatric or neurological symptoms (2-4). Early diagnosis and treatment of anti-NMDAR encephalitis are crucial for improving clinical outcomes. First-line therapies include corticosteroids, intravenous immunoglobulins (IVIG), and plasma exchange with tumor removal, such as teratomas, being necessary if detected. However, studies indicate that approximately half of the patients show poor response to these first-line therapies (1-3). For patients who do not respond adequately to first-line therapy within two to four weeks, second-line treatments, including immunosuppressive drugs like rituximab, cyclophosphamide, azathioprine, or mycophenolate mofetil, are recommended (1,3). Rituximab is a chimeric monoclonal antibody targeting CD20 on B cells, has been associated with better outcomes and fewer relapses (3) in patients with anti-NMDAR encephalitis, leading some experts to recommending it as first-line therapy (1). Additionally, supportive therapies, such as antiepileptic and antipsychotic medications, are used to manage neurological and psychiatric symptoms (1,4).

This report explores a pediatric case of refractory anti-NMDA receptor encephalitis, emphasizing on the unique challenges in diagnosis and management. This case integrates traditional clinical assessments with flow cytometry-based immunophenotyping and detailed symptomatology to offer a nuanced perspective on disease progression. After first-line treatment, the patient was administered rituximab and adjunctive hydrogen therapy. Recent studies suggest that hydrogen therapy activates the nuclear factor 2 erythroid 2 (NRF2) pathway, providing antioxidative and anti-inflammatory benefits that may complement traditional treatment (5-9). The patient showed upregulation of PD-1+ cytotoxic T cells (Tc) and regulatory T cells (Tregs), along with downregulation of B cells, correlating with positive clinical outcomes. These immunophenotyping profiles may reflect the effectiveness of the combined medication, particularly the adjunctive hydrogen therapy. The clinical course, diagnostic approach, and combined interventions in the case highlight the critical role of integrating flow cytometry-based immuno-phenotyping for precise assessment and management. This report was approved by the Institutional Review Board (IRB) of Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan (IRB: C202415137, approval date: 29 July 2024). Written informed consent was obtained from the patient (No. V1-20240712).

Case Report

A 14-year-old male experienced a sudden generalized tonic-clonic seizure with loss of consciousness at school on November 3, 2023, and was initially taken to the Taipei Veterans General Hospital before being transferred to Tri-Service General Hospital. Electrocardiogram and neurological examination, including computed tomography (CT), showed no abnormalities (Figure 1A). However, he soon developed agitation and bizarre behavior, and subsequently presented to our emergency department (ED) on November 4. Upon arrival, he exhibited bizarre behaviors, fever (38.2˚C), and an elevated creatine kinase (CK) level (1,344 U/l), leading to his admission to the SNCU. Levetiracetam was administered to manage seizure symptoms. A central nervous system (CNS) infection, including encephalitis, was ruled out as the CSF obtained via lumbar puncture was clear. Consequently, a series of diagnostic tests including assessments for autoimmune antibodies, viral antibodies, thyroid function, tumor markers, magnetic resonance imaging (MRI) and electroencephalogram (EEG) were conducted to determine the cause of the suspected aseptic meningitis (Table I, Figure 1B and C). The tests revealed the presence of anti-NMDA antibodies in both serum and CSF (Table I, Figure 1D). As a result, therapeutic interventions for anti-NMDA receptor encephalitis and associated epilepsy were initiated (Figure 2). In addition to standard diagnostics and treatments, the patient underwent flow cytometry analysis for immunophenotyping.

Figure 1.

Figure 1

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Clinical evaluation of the case. (A) Brain CT scan performed on November 3, 2023, showed no significant abnormalities. (B) Brain MRI conducted on November 5, 2023, revealed mucus accumulation in the right frontal sinus but was otherwise unremarkable. (C) An EEG on November 6, 2023, showed an abnormal EEG study indicating generalized encephalopathy. (D) A positive NMDAR antibody result (100-fold dilution) was detected in the CSF on November 6, 2023, prior to treatment. CT: Computed tomography; MRI: magnetic resonance imaging; EEG: electroencephalogram; CSF: cerebrospinal fluid.

Table I. Laboratory findings and diagnostic tests in cerebrospinal fluid for suspected aseptic meningitis in the case.

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#1The targets of limbic encephalitis examinations: NMDAR, AMPAR1/2, CASPR2, LGI1, GABAβR, and DPPX. #2Bacteria detection contained Escherichia coli K1, Hemophilus influenzae, Listeria monocytogenes, Neisseria meningitidis, Streptococcus agalactiae, Streptococcus pneumoniae, and Cryptococcus neoformans. #3Virus detection consisted of HHV-6, HPeV, VZV, CMV, H. Enterovirus, and HSV-1 & 2. #4Tumor markers included beta-2 microglobulin, TSH, free T4, AFP, CEA, CA19-9, and PSA.

Figure 2.

Figure 2

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Clinical course and treatment timeline. The blue dots on the gray line represent dates in November. Purple dots and arrows indicate the days on which rituximab was administered. Dates for blood sample collection are marked in red text above the corresponding dots. The lightning symbols on the brain denote the severity of epilepsy, with more lightning indicating greater severity. The timeline below the date line details the combination of treatments, including first and second-line therapies for anti-NMDAR encephalitis, epilepsy management, and hydrogen therapy.

As first-line therapy for anti-NMDAR encephalitis, the patient was treated with intravenous immunoglobulin (IVIG, 0.1 g/kg QD), steroid pulse therapy (methylprednisolone 500 mg BID), and plasma exchange therapy (20 U QD) (Figure 2). Brivaracetam (100 mg BID) was substituted for levetiracetam due to concerns about potential neuropsychiatric adverse effects. Despite these interventions, the patient experienced two seizures with partial impairment of consciousness. Flow cytometry-based immunophenotyping unexpectedly revealed an increase in the percentage of B cells following plasmapheresis. To better control the seizures, lacosamide (50 mg BID) was added to brivaracetam (100 mg BID). Given to the upregulated of B cells (Figure 3E), likely due to a compensatory rebound, plasma exchange therapy was subsequently discontinued.

Figure 3.

Figure 3

Figure 3

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Immunophenotypic profiles of whole blood were analyzed on nine dates: before adjunctive hydrogen therapy (November 6-9, 2023; November 11, 2023) and after therapy (November 13, 2023; November 16, 2023; November 23, 2023; November 28, 2023). (A-D) Show the percentages of PD-1+ expression in central memory Tc cells, naïve Tc cells, effector Tc cells, and effector memory Tc cells before and after adjunctive hydrogen therapy. (E-H) Illustrate the percentages of total B cells, double-negative B cells, naïve B cells, and transitional B cells before and after adjunctive hydrogen therapy. (I-N) Present the percentages of Tregs and their subsets prior to and following adjunctive hydrogen therapy. Abbreviations used are as follows: HC: Healthy control; Tc: cytotoxic T cells (CD3+CD8+); central memory Tc: CD3+ CD8+ CCR7+ CD45RA-; naive Tc: CD3+ CD8+ CCR7+ CD45RA+; effector Tc: CD3+ CD8+ CCR7– CD45RA+; effector memory Tc: CD3+ CD8+ CCR7– CD45RA–; B cells: CD19+; naive B cells: CD19+ CD27– IgD+; double negative B cells: CD19+ CD27– IgD–; transitional B cells: CD19+ IgM+ CD27– CD38+ CD24+; T helper cells: CD3+ CD4+; Treg1: CD3+ CD4+ CD25high; Treg2: CD3+ CD4+ CD25high CD127low/–; FoxP3+ Treg: CD3+ CD4+ CD25high CD127low/-FOXP3high; activated Treg: CD3+ CD4+ CD25high FOXP3high CD45RA–; resting Treg: CD3+ CD4+ CD25high FoxP3low CD45RA+; natural Treg: CD3+ CD4+ CD25high FoxP3+ Helios+.

Since initial treatments proved ineffective, additional therapies were introduced on November 11, including the early administration of rituximab (100 mg), adjunctive hydrogen therapy (1 capsule QD), and prophylactic antibiotics, followed by a second course of IVIG therapy (2 g/kg QD) for refractory anti-NMDAR encephalitis. Adjunctive hydrogen therapy was employed to harness its potential antioxidative and inflammatory effects through NRF2 pathway activation (5,9). Although B cells decreased after rituximab treatment, the patient continued to experience daytime drowsiness, episodic agitation, disinhibited behavior, and stereotypic movements from November 13 to 17. Consequently, both steroid pulse therapy and a scheduled rituximab (100 mg) were then administered again on Nov. 17. Anti-seizure treatments were intensified with brivaracetam (100 mg BID) combined with an increased dose of lacosamide (100 mg BID). Following this combined treatment, the patient’s condition stabilized and he was transferred to the general ward the next day. During this period, rituximab (200 mg) and a third course of IVIG therapy (20 mg daily) were administered. Due to the occurrence of stereotypic movements and impaired consciousness once daily, clonazepam (1 mg daily) was added on November 25, but it was later discontinued due to adverse side effects. Consequently, anti-seizure therapy was adjusted to a combination of brivaracetam (100 mg BID), lacosamide (100 mg BID), and clobazam (5 mg BID). This adjustment led to improvement in epilepsy symptoms and increased verbal output. The patient’s condition remained stable, and he was discharged on November 30 (Figure 2).

In addition to traditional diagnostic methods for anti-NMDAR encephalitis, flow cytometry was employed to analyze the immunophenotyping of immune cell subsets in the whole blood, allowing for observation of dynamic changes during the treatment. The approaches, procedures, and cell gating strategy for immunophenotyping were based on established studies (10,11). Specifically, during the early disease onset (November 6 to 8), a decrease in PD-1+ Tc cells was observed, while B cells and Tregs were increased (Figure 3A-E, I-J). Between November 9 and 1, low levels of PD-1+ Tc, declined Tregs, and upregulated B cells were noted following combined therapy (IVIG, methylprednisolone, plasmapheresis, and epilepsy treatments), indicating a poor therapeutic response. Consequently, plasma exchange therapy was terminated, and rituximab and adjunctive hydrogen therapy were initiated. By November 16 or 23, an upregulation of PD-1+ Tc subsets (naive Tc, central memory Tc, effector Tc, and effector memory Tc) and Treg subsets (Treg, FoxP3+ Treg, activated Treg, resting Treg, and natural Treg) was observed (Figure 3A-D, I-N). Conversely, B cells, particularly naïve B cells, double-negative B cells (DN-B), and transitional B cells, were downregulated (Figure 3E-H). These detailed immune profiles trends may reflect the clinical outcomes in this case of refractory anti-NMDAR encephalitis.

Discussion

This case underscores the complex relationship between clinical symptomatology and immune responses in anti-NMDA receptor encephalitis, highlighting the value of integrating immuno-phenotyping into the clinical assessment. The observed shifts in immune cell populations corresponded with specific clinical manifestations, offering potential biomarkers for disease progression and treatment response. Treatment adjustments could be guided by the integration of the immunophenotypic profile. Notably, a reduction of PD-1, elevated B cells, and decreased Tregs during disease onset were correlated with a poor treatment response, whereas the subsequent downregulation of B cells and the upregulation of PD-1+ Tc subsets following treatments were associated with positive clinical outcomes.

Programmed cell death protein 1 (PD-1) is an immune checkpoint that regulates T cells by modulating their activation, differentiation, and functions. Additionally, of T cells. Additionally, PD-1 influences the induction of Tregs (12). Under normal conditions, PD-1 and Tregs play a crucial role in maintaining immunoregulation and preventing autoimmune overreaction. In this case, early disease onset and initial treatments (IVIG, methylprednisolone, and plasmapheresis) were associated with a decrease in PD-1+ Tc subsets (including naïve Tc, effector Tc, central memory Tc, and effector memory Tc) and Tregs (Figure 3A-D, I-J). Additionally, the frequency of FoxP3+Tregs, natural Tregs and activated Tregs were unstable (Figure 3K, L, and N), suggesting immune system overactivation, which may be linked to the severity of symptoms and indicating the need for medication adjustments. Meanwhile, B cell subsets, which are relevant to anti-NMDAR encephalitis, exhibited significant variations. Both total B cells and specific subsets, such as naïve B cells and DN-B cells, increased during the disease outbreak and periods of suboptimal response periods (Figure 3E-G). Although transitional B cells initially decreased, they sharply increased following the first course of combined therapy on November 11 (Figure 3H). Consequently, medication adjustments were made based on both clinical and immunophenotypic evaluations, resulting in replacement of plasma exchange therapy with rituximab.

The early use of rituximab, guided by regular immuno-phenotyping evaluations, along with adjunctive hydrogen therapy, ultimately improved the patient’s condition. Hydrogen therapy activates the NRF2 pathway, leading to increased expression of antioxidant proteins and enzymes that mitigate oxidative stress and inflammation, suggesting its potential utility in managing autoimmune conditions and other diseases, such as chronic kidney disease, non-alcoholic fatty liver disease, alcohol intoxication, neurodegenerative disorders, and immunoglobulin G4-related progressive fibrosing interstitial lung disease (5-7,9,11). In this case, the addition of hydrogen capsules contributed to stabilizing the patient’s condition by modulating immune cell subsets and reducing oxidative damage. Rituximab, an anti-CD20 monoclonal antibody, has been shown to decrease the frequency of B cells, including naïve B cells and unswitched memory B cells, in lymph node biopsies (13). Notably, as the patient’s condition improved with the combined therapy of hydrogen therapy and rituximab, there were significant changes in immunophenotypic markers. Specifically, PD-1+ in Tc subsets (Figure 3A-D) was upregulated correlating with improved symptoms. Additionally, Tregs, including FoxP3+Tregs, resting Tregs, natural Tregs, and activated Tregs increased (Figure 3I-N), while B cells, including naïve B cells, DN-B cells, and transitional B cells, decreased (Figure 3E-H) during the steady state of the disease. These observations aligned with the positive response to treatment, indicating that the immunophenotypic profiles accurately reflected the therapeutic response. Moreover, prior reports have demonstrated that adjunctive hydrogen therapy elevates resting Tregs, thereby enhancing treatment outcomes in autoimmune diseases (11). Similarly, increased levels of Tregs have been observed in patients with refractory myasthenia gravis following rituximab treatment (14).

The N-methyl-D-aspartate receptor (NMDAR) is a crucial excitatory receptor involved in neurotransmitter signaling within the CNS. Studies suggest that the pathological mechanism of anti-NMDAR encephalitis may originate from tumors, particularly ovarian teratomas, or from viral infections, such as herpes simplex virus 1 or even SARS-CoV-2. Naïve B cells can differentiate into memory B cells upon exposure to NMDAR, potentially facilitated by tumor antigens or neuronal debris released during viral infections. There are two proposed pathways for the production of anti-NMDAR antibodies by memory B cells. One pathway involves the differentiation of memory B cells into plasma cells within the CNS, where they secrete pathogenic antibodies against NMDAR. The other involves peripheral plasma cells releasing anti-NMDAR antibodies that subsequently cross into CNS (15-17). Despite these insights, the etiology remains unidentified in most patients with anti-NMDAR encephalitis, including our case. Nonetheless, B cells play a critical role in the disease, as they are the primary producers of antibodies. The NR1 subunit of NMDAR is the major target of these IgG autoantibodies, and it has been suggested that naïve B cells are closely associated with the production of NR1 autoantibodies (18). Moreover, patients with anti-NMDAR encephalitis exhibit elevated levels of IgD-CD27- double negative B cells (19), consistent with our findings (Figure 3F). In addition to B cells, our case’s immune profiling indicated that dysregulated PD-1 expression and Tregs may contribute to the poor response seen in anti-NMDAR encephalitis. Although evidence regarding the role of PD-1 in anti-NMDAR encephalitis is limited, some studies suggest that PD-1 inhibitors can trigger the onset of autoimmune encephalitis (20). Moreover, researchers has shown that dysregulated Tregs are a common feature in autoimmune diseases (21), with patients suffering from anti-NMDAR encephalitis exhibiting lower Tregs levels compared to healthy controls (22). In our case, both B cells and PD-1+ Tc and Tregs subsets emerged as potential markers for monitoring disease progression and treatment response.

To sum up, although the underlying mechanism of anti-NMDAR encephalitis are not yet fully understood, integrating clinical symptomatology with immunophenotypic analysis via flow cytometry enhances our understanding of the disease. This comprehensive approach aids in the selection of appropriate treatment strategies and the timing of therapeutic adjustments. Notably, adjunctive hydrogen therapy has shown promising in modulating immune responses and improving treatment efficacy.

Conclusion

In conclusion, this case report highlights the importance of integrating flow cytometry-based immunophenotyping into the assessment and treatment of anti-NMDAR encephalitis. By combining clinical and immunological profiles, personalized treatment strategies such as the incorporation of traditional therapies with innovative interventions like hydrogen therapy present a promising approach for enhancing patient outcomes. The observed variations in immune cell subsets, including PD-1+Tc, B cells, and Tregs at different stages of the disease provide valuable insights for precise evaluation, facilitating timely and tailored treatment decisions. Further research is needed to validates these findings and explore their broader applications in autoimmune encephalitis and other related disorders.

Conflicts of Interest

The Authors declare no conflicts of interest relevant to this research.

Authors’ Contributions

SCL: Writing, review and editing. Validation, data curation, conceptualization. JWL: Writing, review and editing. Validation, data curation, conceptualization. TCL: Writing, review and editing. Validation, data curation, conceptualization. YFS: Writing, review and editing. Data curation. YJH: Writing, review and editing. Data curation. FMW: Writing, review and editing. Resources, conceptualization. SWL: Writing, review and editing. Conceptualization. TYH: Writing, review and editing. Conceptualization. KYW: Writing, review and editing. Conceptualization. FCL: Writing, review and editing. Writing, original draft. Resources, investigation, data curation, conceptualization.

Acknowledgements

This study was supported by the Ministry of Science and Technology (MOST 109-2314-B-016-052 and MOST 111-2314-B-016-026), the National Science and Technology Council (NSTC 112-2314-B-016-033, NSTC 113-2314-B-016-052), and Tri-Service General Hospital (TSGH-E-111215, TSGH-E-112218) in Taiwan.

References

  • 1.Samanta D, Lui F. Anti-nmdar encephalitis. Treasure Island, FL, USA, Statpearls. 2024 [PubMed] [Google Scholar]
  • 2.Dalmau J, Armangué T, Planagumà J, Radosevic M, Mannara F, Leypoldt F, Geis C, Lancaster E, Titulaer MJ, Rosenfeld MR, Graus F. An update on anti-NMDA receptor encephalitis for neurologists and psychiatrists: mechanisms and models. Lancet Neurol. 2019;18(11):1045–1057. doi: 10.1016/S1474-4422(19)30244-3. [DOI] [PubMed] [Google Scholar]
  • 3.Nguyen L, Wang C. Anti-NMDA receptor autoimmune encephalitis: diagnosis and management strategies. Int J Gen Med. 2023;16:7–21. doi: 10.2147/IJGM.S397429. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Lin KL, Lin JJ. Neurocritical care for Anti-NMDA receptor encephalitis. Biomed J. 2020;43(3):251–258. doi: 10.1016/j.bj.2020.04.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Zheng CM, Hou YC, Liao MT, Tsai KW, Hu WC, Yeh CC, Lu KC. Potential role of molecular hydrogen therapy on oxidative stress and redox signaling in chronic kidney disease. Biomed Pharmacother. 2024;176:116802. doi: 10.1016/j.biopha.2024.116802. [DOI] [PubMed] [Google Scholar]
  • 6.Wu HT, Tsai CS, Chao TH, Ou HY, Tsai LM. A novel antioxidant, hydrogen-rich coral calcium alters gut microbiome and bile acid synthesis to improve methionine-and-choline-deficient diet-induced non-alcoholic fatty liver disease. Antioxidants (Basel) 2024;13(6):746. doi: 10.3390/antiox13060746. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Wu HT, Chao TH, Ou HY, Tsai LM. Coral hydrate, a novel antioxidant, improves alcohol intoxication in mice. Antioxidants (Basel) 2022;11(7):1290. doi: 10.3390/antiox11071290. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Chiu SH, Douglas FL, Chung JR, Wang KY, Chu CF, Chou HY, Huang WC, Wang TY, Chen WW, Shen MC, Liu FC, Hsiao PJ. Evaluation of the safety and potential lipid-lowering effects of oral hydrogen-rich coral calcium (HRCC) capsules in patients with metabolic syndrome: a prospective case series study. Front Nutr. 2023;10:1198524. doi: 10.3389/fnut.2023.1198524. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Ohta S. Molecular hydrogen may activate the transcription factor nrf2 to alleviate oxidative stress through the hydrogen-targeted porphyrin. Aging Pathobiol Ther. 2023;5(1):25–32. doi: 10.31491/apt.2023.03.104. [DOI] [Google Scholar]
  • 10.Lui SW, Hsieh TY, Lu JW, Chen YC, Lin TC, Ho YJ, Liu FC. Predicting the clinical efficacy of JAK inhibitor treatment for patients with rheumatoid arthritis based on Fas+ T cell subsets. APMIS. 2023;131(9):498–509. doi: 10.1111/apm.13341. [DOI] [PubMed] [Google Scholar]
  • 11.Lui SW, Lu JW, Ho YJ, Tang SE, Ko KH, Hsieh TY, Liu FC. Molecular hydrogen as a promising therapy could be linked with increased resting treg cells or decreased Fas+ T cell subsets in a IgG4-PF-ILD patient: a case report. In Vivo. 2024;38(3):1512–1518. doi: 10.21873/invivo.13600. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Jubel JM, Barbati ZR, Burger C, Wirtz DC, Schildberg FA. The role of PD-1 in acute and chronic infection. Front Immunol. 2020;11:487. doi: 10.3389/fimmu.2020.00487. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Ramwadhdoebe TH, van Baarsen LGM, Boumans MJH, Bruijnen STG, Safy M, Berger FH, Semmelink JF, van der Laken CJ, Gerlag DM, Thurlings RM, Tak PP. Effect of rituximab treatment on T and B cell subsets in lymph node biopsies of patients with rheumatoid arthritis. Rheumatology (Oxford) 2019;58(6):1075–1085. doi: 10.1093/rheumatology/key428. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Jing S, Lu J, Song J, Luo S, Zhou L, Quan C, Xi J, Zhao C. Effect of low-dose rituximab treatment on T- and B-cell lymphocyte imbalance in refractory myasthenia gravis. J Neuroimmunol. 2019;332:216–223. doi: 10.1016/j.jneuroim.2019.05.004. [DOI] [PubMed] [Google Scholar]
  • 15.Huang Q, Xie Y, Hu Z, Tang X. Anti-N-methyl-D-aspartate receptor encephalitis: A review of pathogenic mechanisms, treatment, prognosis. Brain Res. 2020;1727:146549. doi: 10.1016/j.brainres.2019.146549. [DOI] [PubMed] [Google Scholar]
  • 16.Lee DSW, Rojas OL, Gommerman JL. B cell depletion therapies in autoimmune disease: advances and mechanistic insights. Nat Rev Drug Discov. 2021;20(3):179–199. doi: 10.1038/s41573-020-00092-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Nabizadeh F, Balabandian M, Sodeifian F, Rezaei N, Rostami MR, Naser Moghadasi A. Autoimmune encephalitis associated with COVID-19: A systematic review. Mult Scler Relat Disord. 2022;62:103795. doi: 10.1016/j.msard.2022.103795. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Wenke NK, Kreye J, Andrzejak E, van Casteren A, Leubner J, Murgueitio MS, Reincke SM, Secker C, Schmidl L, Geis C, Ackermann F, Nikolaus M, Garner CC, Wardemann H, Wolber G, Prüss H. N-methyl-D-aspartate receptor dysfunction by unmutated human antibodies against the NR1 subunit. Ann Neurol. 2019;85(5):771–776. doi: 10.1002/ana.25460. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Li S, Hu X, Wang M, Yu L, Zhang Q, Xiao J, Hong Z, Zhou D, Li J. Single-cell RNA sequencing reveals diverse B cell phenotypes in patients with anti-NMDAR encephalitis. Psychiatry Clin Neurosci. 2024;78(3):197–208. doi: 10.1111/pcn.13627. [DOI] [PubMed] [Google Scholar]
  • 20.Feng S, Coward J, McCaffrey E, Coucher J, Kalokerinos P, O’Byrne K. Pembrolizumab-induced encephalopathy: A review of neurological toxicities with immune checkpoint inhibitors. J Thorac Oncol. 2017;12(11):1626–1635. doi: 10.1016/j.jtho.2017.08.007. [DOI] [PubMed] [Google Scholar]
  • 21.Shin YW, Lee ST, Park KI, Jung KH, Jung KY, Lee SK, Chu K. Treatment strategies for autoimmune encephalitis. Ther Adv Neurol Disord. 2017;11:1756285617722347. doi: 10.1177/1756285617722347. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Li Y, Zhang J, Liu L, Cui S, Sun H, Jiang H, Guo Y, Zhang J, Xie Z, Wang J. The imbalance between Bregs, Tfh, and Tregs in patients with anti-N-methyl-D-aspartate receptor encephalitis. Neurol Sci. 2023;44(7):2465–2474. doi: 10.1007/s10072-023-06624-z. [DOI] [PMC free article] [PubMed] [Google Scholar]

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