Proteomics confirms immune stabilizing effects of narrowband UVB treatment in patients with clinically isolated syndrome and multiple sclerosis

Prue H Hart^a Pr*******@*********rg.au ∙ Christopher J Emig^b,c ∙ Ahmed Z Obeidat^d ∙ Stephanie Trend^a,e ∙ Allan G Kermode^e,f ∙ Ferhan Qureshi^g ∙ John MacMahon

Abstract

Background: Multiple sclerosis (MS) demonstrates a latitude gradient in prevalence and severity, implicating ultraviolet B (UVB) exposure and photoimmune mechanisms in disease risk and progression. While narrowband (NB)-UVB phototherapy has long stabilized inflammation in dermatology, its systemic immunomodulatory effects in MS remain incompletely defined. Objective To characterize the photoimmune impact of NB-UVB in clinically isolated syndrome (CIS)/MS patients, leveraging untargeted and targeted proteomic analysis including the Octave Multiple Sclerosis Disease Activity Score. Methods In the PhoCIS trial, CIS patients were randomized to NB-UVB (3 × /week for 8 weeks) or standard care. Serum samples from baseline and day 90 were analyzed using the Olink Target 96 Inflammation panel (untargeted) and the clinically validated MS Disease Activity (MSDA) test panel (targeted). Statistical analyses compared differences within and between-groups. Results Comparing the difference from baseline to day 90, the NB-UVB cohort had significant downregulation in 23 of 92 inflammatory proteins, while the Controls had no changes. Targeted MSDA scores confirmed similar differentially significant reductions in general disease activity and severity, and within the component neuroinflammation, immunomodulation, and neuroaxonal integrity scores. Conclusion NB-UVB caused broad and coordinated reductions in untargeted and targeted inflammatory proteins. These effects support NB-UVB as a promising immunomodulatory strategy in MS in both general inflammation and MS-specific activity, as well as consideration of inflammatory markers and the MS Disease Activity Score as surrogate endpoints in future trials.

Keywords

1 Introduction

MS is a heterogeneous disease with many genetic and environmental factors contributing to disease initiation, progression, and clinical symptoms. Latitude gradients for MS prevalence (more disease for populations living at higher latitudes (Simpson et al., 2019) and disease severity, (Ostkamp et al., 2021; Wu et al., 2024) are well accepted suggesting that sun exposure and the biomolecules that the skin produces upon sun exposure, may contribute to pathways associated with MS development and progression. Many studies have implicated vitamin D, which is produced in skin upon exposure to UVB radiation, as important in balancing the immune system and determining MS outcomes, with vitamin D deficiency listed as one of the most important risk factors for MS. (Munger et al., 2006)

Outcomes of Vitamin D supplementation in patients with Clinically Isolated Syndrome (CIS) or multiple sclerosis (MS), as in other autoimmune diseases, have, however, been disappointing and often contradictory. (Hupperts et al., 2019; Smolders et al., 2019) Any improvements in disease activity with vitamin D supplementation have been small. In consideration of the development of the disease, in the PrevANZ study of 204 patients with CIS randomized 1:1:1:1 to placebo, 1000, 5000 or 10,000 IU oral vitamin D daily for 48 weeks, the intervention had no impact on MS development. (Butzkueven et al., 2024) In the recently reported d-Lay MS clinical trial, where 163 patients with CIS were administered 100,000 IU of vitamin D every 2 weeks for 24 months, there was a reduction in disease activity in CIS and early relapsing-remitting MS. (Thouvenot et al., 2025) However, the biological basis for such high, non-physiological pulsed doses of vitamin D requires clarification.

Multiple biologically active, immunoregulatory molecules are made in skin upon UVR exposure (for review, (Bernard et al., 2019; Hart et al., 2011; Slominski et al., 2024)). The immunomodulation that occurs following UVR exposure has clear medical benefits for some inflammatory conditions, including graft-versus-host disease, and NB-UVB has been used for decades in the treatment of patients with inflammatory skin conditions in a manner that does not increase skin cancer incidence. To evaluate the effectiveness of NB-UVB in slowing the progression from clinically isolated syndrome to MS, the PhoCIS trial (narrowband UVB Phototherapy for CIS) was established using similar NB-UVB protocols as had been used for the treatment of psoriasis and other inflammatory conditions.

The aims and clinical outcomes of the PhoCIS trial have been published. (Hart et al., 2017, 2018) All participants had been diagnosed with CIS, within 120 days of entering the trial. Participants were randomized into two groups, with the treated group receiving suberythemal NB-UVB three times per week over 8 weeks, a conservative dose schedule within dermatological guidelines and clinical trials, where improved outcomes have been confirmed with treatment regimens for up to 24 weeks and the other group was treated with standard of care. (Gelfand et al., 2024) After 12 months, all participants who did not receive NB-UVB had converted to clinically definite MS, whilst 70 % of those receiving NB-UVB had progressed from CIS to MS. (Hart et al., 2018) However, the clinical outcomes were not significant due to the low number of participants (n = 20). Subsequent studies on biobanked cells and sera from the participants have suggested benefit of exposure to NB-UVB to disease pathogenesis. Compared with the CIS participants who did not receive NB-UVB, there was a reduction in the percentage of circulating switched memory B cells and an increase in the percentage of naïve B cells in the treated group. (Trend et al., 2019) There was also a reduction in the ability of B cells to make the inflammatory mediator TNFα upon polyclonal activation in vitro, (Trend et al., 2020) as well as a stabilization in the ability of peripheral blood mononuclear cells to express Arginase1. (Cha et al., 2018) In addition, the participants given NB-UVB self-reported increased social functioning and reduced fatigue. (Hart et al., 2018) Thus, PhoCIS could be described as a small trial with a conservative NB-UVB dosing regimen, with outcomes suggestive of NB-UVB’s benefit to a subset of patients with CIS. The 2017 revisions to the McDonald criteria for MS have significantly broadened the diagnostic criteria. (Gaetani et al., 2018; van der et al., 2018) Consequently, the PhoCIS trial data is now applicable to a wider range of MS patients. The inclusion of CSF oligoclonal bands assessments has been a key driver of this change, as 54–82 % of patients with Clinically Isolated Syndrome (CIS) now meet MS criteria at baseline, compared to the previous criteria.

In this study, more objective serum markers were investigated to determine a basis for the beneficial effects of narrowband UVB phototherapy on disease activity and progression of CIS/MS patients.

2 Materials and methods

2.1 Materials

Serum samples from patients with CIS (n = 20) were obtained from the PhoCIS trial. All participants were naïve to MS disease-modifying therapy and had not received steroids for more than 30 days. The PhoCIS study was approved by the Bellberry Human Research Ethics Committee (2014–02–082) and endorsed by the Human Research Ethics Office of the University of Western Australia (RA/4/1/6796) (ACTRN 12,614,000,185,662). Serum samples taken from participants on the first day of their involvement in the trial (day 0) and after 90 days were analyzed with a focus on within-group changes over 90 days, and between-cohort differences in longitudinal protein expression.

2.2 Methods

Biobanked sera were analyzed by both untargeted and targeted assays performed using proximity extension assay (PEA) technology (Olink Proteomics, Uppsala, Sweden), a high-sensitivity platform validated for multiplexed protein quantification in serum.

Untargeted proteomics used the Olink Target 96 Inflammation Panel, which quantifies 92 inflammation-associated proteins with high reproducibility (intra-assay CV: 5–12 %, inter-assay CV: 11–21 %) and specificity. Untargeted pathway analysis was performed with Gene Set Enrichment Analysis (GSEA) using WEB-based GEne SeT AnaLysis Toolkit (WebGestalt) against the WikiPathways database. (Agrawal et al., 2024; Liao et al., 2019)

Targeted proteomics utilized the MS Disease Activity (MSDA) test panel (Octave Bioscience, Menlo Park, CA), which assayed 18 proteins. Algorithms have been validated for measurement of the analytes to generate an MS Disease Activity Score (MSDA) that predicts new gadolinium enhancing (Gd+) MRI lesions, new and enlarging T2 MRI lesions, and active/stable status (composite endpoint combining radiographic and clinical indicators of disease activity) in MS patients. (Chitnis et al., 2023) Scores for 4 contributory pathways relevant to MS pathogenesis (immunomodulation, neuroinflammation, myelin biology and neuroaxonal integrity), were generated. (Chitnis et al., 2023) The general score (1–10 scale) associates with increasing severity, with ratings of low (1.0–4.0), moderate (4.5–7.0), and high (7.5–10.0). The severity ratings have been clinically validated against gadolinium-enhancing (Gd+) lesion risk. (Chitnis et al., 2023)

2.3 Statistical analysis

Olink and MSDA Score statistical analyses were conducted using Python (version 3.8.19). Data processing and visualization were performed with standard scientific libraries, including pandas, numpy, scipy, statsmodels, matplotlib and seaborn. Due to the nuances of small n, different statistical tests are included for analytes and pathways. Statistical significance for within-group changes (Day 90 vs. Day 0) was evaluated using a two-sided paired Student’s t-test (p < 0.05). For between-cohort analysis, the net change at Day 90 (“Day90Δ”) for each participant was calculated by subtracting the Day 0 (“baseline”) measurements from Day 90 measurements. Differences in Day90Δ between NB-UVB and control cohorts were evaluated using a one-sided, independent t-test, with significance defined as P < 0.05. Welch’s t-test was used for Olink significance calculations because of the large difference in the paired sample counts between NB-UVB and control cohorts.

Fisher’s Exact Tests were used for the MSDA severity categorical variable, from between and within-group 2 × 3 contingency tables. The MSDA severity scores were categorized according to the risk for the participant to develop new Gd+ lesions. Student’s t-test was used for MSDA score significance calculations. The use of one-sided t-tests between cohorts was justified because our hypothesis was unidirectional (NB-UVB treatment would decrease levels of inflammatory markers relative to the control group).

3 Results

3.1 Untargeted inflammatory mediators in serum using an Olink inflammation panel

Analysis of serum analytes using the Olink Inflammation Panel was performed in a blinded fashion on paired serum samples from 7 CIS participants receiving NB-UVB and 3 CIS participants who were controls, as they did not receive NB-UVB. The concentration of analytes in serum taken after 90 days was subtracted from those measured in serum from the same individual at the start of the trial (day 0)(“D90Δ”). Serum analytes whose levels were significantly changed between day 0 and day 90 in the control cohort are shown in Fig. 1A (all increases), while serum analytes whose levels significantly changed between day 0 and day 90 in both the control (all increases) and NB-UVB cohorts (all decreases) are seen in Fig. 1B Fig. 1C shows serum analytes whose levels changed significantly between day 0 and day 90 in the NB-UVB cohort and did not vary significantly in serum samples from the control cohort. Pathway analyses concentrated on the 23 analytes that were reduced by NB-UVB. All could be grouped into five biologically relevant processes: cytokine signaling and inflammation, chemokine networks and immune cell migration, the TNF superfamily and apoptosis, growth factors and tissue remodeling, and cellular signaling regulators. The functions of these analytes are shown in Supplementary Table 1.

Fig 1 — **Fig. 1** Analytes significantly altered from time 0 levels in the serum of PhoCIS participants at 90 days using the Olink Inflammation Panel. Levels of 92 analytes were measured in paired samples from 7 participants receiving NB-UVB and 3 participants not receiving NB-UVB (Controls). Serum analytes were filtered by those for which levels significantly changed at 90 days in the treatment or control group (D90Δ P value<0.05). A. Significantly changed analytes in the Control group, B. Analytes significantly changed in both the Control group and the NB-UVB group, and C. Analytes significantly changed in the NB-UVB group. Box plots show median, the first and third quartile values, whiskers show the minimum and maximum values within 1.5X the IQR. All data points are shown (coloured dots). The statistical significance when comparing the differences over time between the NB-UVB and Control cohorts are shown (*P < 0.05, ** P < 0.01, P < 0.001).

3.2 Pathway enrichment analysis of data from Olink inflammation panel

Gene Set Enrichment Analysis (GSEA) of all 92 serum analytes with in the Olink 96 panel analyses comparing Day 90 to baseline samples, revealed one pathway that was statistically significantly altered (performed with GSEA Webgestalt https://www.webgestalt.org/results/1746634826/#). The WikiPathway WP4329: miRNA role in immune response in sepsis was significantly increased (P < 0.05) (Supplementary Figure 1). The normalized enrichment score (NES) was 1.97, P value 0.002, pathway size 7 genes (all in the leading edge and including TNF, IL1α, IL10, CCL3, CCL4, IL6, and CXCL8). miRNAs typically function by suppressing gene expression. (Antonakos et al., 2022; Bindayna, 2024; Giza and Fuentes-Mattei, 2016) Thus, this pathway represents miRNA-mediated regulation of inflammatory responses, particularly during systemic inflammation. The positive NES (1.97) indicates significant pathway enrichment, while the negative scores for component genes suggest coordinated downregulation of pro-inflammatory mediators. This pattern may reflect an immunomodulatory effect of NB-UVB through potential upregulation of anti-inflammatory miRNAs that suppress these target genes. (Antonakos et al., 2022; Bindayna, 2024; Giza and Fuentes-Mattei, 2016)

3.3 Inflammatory mediators within the disease activity assessments in MS

The Olink-generated data suggested an anti-inflammatory effect of NB-UVB that persisted for 30 days beyond the 60-day treatment period. To obtain more informative data, paired serum samples from 9 PhoCIS participants receiving NB-UVB and 8 with CIS but who were not given NB-UVB treatment were then analyzed using an MS-targeted serum proteomic assay. (Chitnis et al., 2023) Samples taken after 90 days were again compared with those taken at time 0 from the same participant. Importantly, this assay of 18-proteins has been validated based on associations between algorithm score and clinical/radiographic assessments of patients with MS and trained based on the presence/absence of gadolinium-positive (Gd+) lesions. (Chitnis et al., 2023)

The measurement of the 18 serum proteins allowed the calculation of a MS Disease Activity Score (MSDA). (Chitnis et al., 2023) At time 0, there was no difference between the MSDA scores for the CIS cohorts who received NB-UVB and those who did not (Fig. 2, Table 1). After 90 days, on average, the difference in MSDA scores was 1.7 points lower (out of 10) with NB-UVB treatment vs. participants in the control arm (P = 0.01, paired t-tests). When the MSDA scores were broken down into the 4 activity pathways (Fig. 2, Table 1, Chitnis et al., 2023) the scores for immunomodulation, neuroinflammation, and neuroaxonal Integrity were significantly reduced, but not that for myelin biology.

Fig 2 — **Fig. 2** Diffferences in MSDA scores, and scores for the component pathways, Immunomodulation, Neuroinflammation, Myelin Biology, and Neuroaxonal Integrity, measured in the serum of PhoCIS participants at both 0 and at 90 days. MSDA scores were calculated from the levels of 18 analytes measured in paired samples (time 0 and after 90 days) from 9 participants who were treated with NB-UVB, and 8 participants with CIS and given standard care (Controls). Box plots show median, the first and third quartile values, whiskers show the minimum and maximum values within 1.5X the IQR. All data points are shown (colored dots). The statistical significance when comparing the differences over time between the NB-UVB and Control cohorts are shown (*P < 0.05, ** P < 0.01).

MSDA Pathway	Control Day 0	Control Day 90	Δ Control	NB-UVB Day 0	NB-UVB Day 90	Δ NB-UVB	Δ NB-UVB -Δ Control	NB-UVB vs. Control p-value
General Score	6.3	7.1	0.9	6.7	5.9	−0.8	−1.7	0.010
Immunomodulation Score	6.9	8.2	1.3	7.4	6.9	−0.5	−1.8	0.006
Myelin Biology Score	6.7	6.8	0.1	7.3	6.7	−0.6	−0.7	0.157
Neuroaxonal Integrity Score	5.7	6.1	0.4	5.3	3.9	−1.4	−1.8	0.047
Neuroinflammation Score	6.1	7.2	1.1	8.0	7.0	−1.0	−2.1	0.007
								* one-sided Student’s t-tests

Table 1

MS disease activity scores for paired sera (Day 0 and Day 90) from 9 CIS participants who received NB-UVB treatment and 8 CIS participants who received standard of care (Controls). Scores for the four pathways that contribute to the MS Disease Activity Score are also shown.

Open table in a new tab

3.4 MSDA scores and MS severity

The MSDA scores of 1.0 to 4.0 have been rated as having a low risk of increased disease activity. Scores of 4.5 to 7.0 have been rated as moderate risk, and 7.5–10.0 as high risk for more severe disease. The odds of having ≥1 new Gd+ lesions with a moderate/high MSDA score have been calculated to be 4.49 times that of a low MSDA score, and the odds of having ≥2 new Gd+ lesions with a high MSDA score are 20.99 times that of a low/moderate MSDA score. (Chitnis et al., 2023)

On average, the 3-month difference in MSDA scores was 1.73 points lower with UVB treatment compared to patients in the control arm (p-value = 0.009).

When the MSDA scores for the participants of the PhoCIS trial were examined by severity category, the serum from the participants in both cohorts at day 0 suggested similar disease activity, notably 57 % and 50 % of the control and NB-UVB groups, respectively, and were in the moderate risk category (Fig. 3). After 90 days, the majority of those in the control group (63 %) had MSDA scores suggesting high disease severity with likely increased Gd+ lesions. By comparison, only 11 % of those who had received NB-UVB treatment had MSDA scores at 90 days suggestive of high disease severity. The majority of those receiving NB-UVB (89 %) could be defined at 90 days of moderate risk for more Gd+ lesions (Fig. 3).

Fig 3 — **Fig. 3** MSDA scores for serum from the participants of the PhoCIS trial examined by Severity Category at Day 0 and after 90 days. MSDA scores were calculated from the levels of 18 analytes measured in paired samples (Day 0 and after Day 90) from 9 participants who were treated with NB-UVB, and 8 participants with CIS and given standard care (Controls). MSDA scores were categorized according to the risk for the participant to develop new Gd+ lesions. Fisher’s Exact Test p-values for each 2 × 3 Contingency Table.

4 Discussion

This study provides preliminary but compelling evidence that NB-UVB phototherapy exerts a broad anti-inflammatory effect in patients with CIS/MS, as measured by a 92 analyte, untargeted Olink Inflammation Panel, and the more targeted 18 analyte proteomic platform that allows calculation of MSDA scores. Findings of changes to the serum proteome complement previously published findings from participants of the PhoCIS study receiving NB-UVB. (Hart et al., 2018) Previous analyses of both the number and function of blood cells from the participants receiving NB-UVB suggested a down-regulation of inflammatory processes potentially associated with MS development. (Trend et al., 2019, 2020) Greater knowledge of the mechanisms of action of NB-UVB has been called by several international groups (Alfredsson et al., 2020; Ostkamp and Schwab, 2022) and may aid in its acceptance for the treatment of MS.

Results from the Olink Inflammation Panel suggested a broad anti-inflammatory effect of NB-UVB, with downregulation of multiple cytokine classes including pro-inflammatory cytokines (TNF, IL1α, IL6), chemokines (CCL3, CCL4, CXCL8) and regulatory cytokines (IL10). In contrast, no analytes from the control cohort showed significant decreases in D90Δ values. No analytes from the NB-UVB treatment cohort showed significant upregulation for D90Δ values. The NB-UVB treatment cohort demonstrated reductions in inflammatory mediators not only with respect to their matched day 0 samples, but additionally with respect to the same time point as the control cohort. Overall, this suggests that downregulation of inflammatory mediators is associated with treatment, and progression of inflammatory processes occurs in the absence of treatment. The GSEA results revealed significant positive enrichment of the “miRNA role in immune response in sepsis” pathway following NB-UVB therapy at Day 90 compared to baseline. This pathway represents miRNA-mediated regulation of inflammatory responses, particularly during systemic inflammation. The consistent negative scores for inflammatory mediators suggest NB-UVB therapy induces sustained resolution of inflammatory responses by Day 90, potentially through epigenetic mechanisms involving miRNA regulation. (Antonakos et al., 2022) This aligns with current understanding of miRNAs as regulators of both pro-inflammatory and anti-inflammatory processes in immune responses. (Giza and Fuentes-Mattei, 2016)

The results suggest that exposure to NB-UVB induces balanced immunomodulation. While most downregulated genes are pro-inflammatory, the reduction in IL10 (an anti-inflammatory cytokine) suggests a restoration of immune homeostasis rather than general immunosuppression, consistent with the dual-phase model of inflammation where miRNAs play different roles during early (hyper-inflammatory) and late (immunosuppressive) phases. (Antonakos et al., 2022) Furthermore, these results implicate NB-UVB in immune resolution of inflammatory responses, an effect that was maintained for 30 days after the end of the exposures to NB-UVB at 60 days. This analysis provides molecular evidence that NB-UVB therapy modulates inflammatory responses through pathways originally characterized in sepsis, highlighting potential shared mechanisms between acute systemic inflammation and chronic inflammatory conditions. This result is consistent with the findings in a trial to reduce acute mortality in hospitalized COVID-19 patients and in patients with refractory Graft versus Host Disease. (Fachler-Sharp et al., 2024; Lau et al., 2022) Key components of this miRNA driven pathway have previously been cited in the NB-UVB literature for psoriasis. (Ele-Refaei and El-Esawy, 2015; Soonthornchai et al., 2021)

The more targeted analysis of MSDA scores highlighted the relevance of the anti-inflammatory effects of NB-UVB to the development of MS. NB-UVB therapy led to consistent and significant reductions across several MSDA pathways at day 90 (Table 1). These effect sizes are substantial and, notably, are not matched by the control group, which showed increases in all pathway scores. Severity category analysis further underscores the impact of NB-UVB within and between groups (Fig. 3).

The MSDA panel, now rapidly gaining clinical adoption, is the most robustly validated MS-specific proteomic tool, with strong performance in detecting radiographic disease activity and correlating with clinical outcomes. MSDA scores have been reported in other randomized trials including the Phase 3 ULTIMATE I and II studies where patients with relapsing forms of MS were treated with ublituximab (anti CD20) and as an active comparator, teriflunomide. (Steinman et al., 2022) (manuscript in preparation). Reductions in MSDA scores with ublituximab closely paralleled improvements in clinical and MRI outcomes, supporting the clinical sensitivity of the MSDA assay (manuscript in preparation). With no significant change in the MSDA score with teriflunomide, statistically significant reductions in MSDA scores with NB-UVB must be highlighted. Nonetheless, the small sample sizes and relatively short follow-up in the PhoCIS study, as well as the lack of long-term data of those given NB-UVB, limit the generalizability of these findings. The absence of direct MRI or clinical endpoints in this analysis is another important limitation, though the consistency across MSDA domains and severity categories strengthens the biological signal.

Importantly, these data also provide insights into the photoimmune response embedded in the well-established latitude gradient in MS, suggesting that systemic anti-inflammatory effects of UVB exposure, beyond vitamin D synthesis, may contribute to the observed epidemiological patterns. The effects of NB-UVB in the PhoCIS trial reflect the growing body of evidence supporting the hypothesis that healthy sun exposure habits have tangible protective benefits in MS progression. (Riedmann et al., 2025; Wu et al., 2024) This study also supports the potential use of NB-UVB as an adjunctive therapy with other prescribed Disease Modifying Treatments for MS, particularly as ‘At-Home NB-UVB phototherapy’ has been shown as efficacious, and more acceptable to patients, as phototherapy delivered in a clinic for psoriasis. (Gelfand et al., 2024) These results build on the growing research that the photoimmune cascade initiated by NB-UVB has reach well beyond the confines of the skin.

5 Conclusion

In summary, NB-UVB therapy demonstrated robust, multi-pathway anti-inflammatory effects and a systemic homeostatic response in CIS/MS patients. These results, when considered alongside the strong validation and emerging clinical adoption of the MSDA assay, justify further investigation of NB-UVB as a potential adjunctive therapy in early MS, ideally in larger studies with extended follow-up and clinical endpoints.

Prior presentation

A version of Fig. 3 was presented in a talk by PHH at the International Conference on Sun Exposure and Human Health, Sunshine Health Foundation, Washington DC, May 2024, and the International Photobiology conference, Perth, Australia, August 2024. A version of Fig. 3 was presented in a poster by AZO at the Consortium of MS Centres meeting, Nashville, June 2024.

Declaration of generative AI and AI-assisted technologies in the writing process

None.

CRediT authorship contribution statement

Prue H Hart: Data curation, Formal analysis, Funding acquisition, Methodology, Project administration, Supervision, Writing – original draft, Writing – review & editing. Christopher J Emig: Data curation, Formal analysis, Methodology, Validation, Visualization, Writing – review & editing. Ahmed Z Obeidat: Formal analysis, Methodology, Validation, Writing – review & editing. Stephanie Trend: Methodology, Project administration. Allan G Kermode: Investigation, Methodology. Ferhan Qureshi: Data curation, Formal analysis, Methodology, Visualization. John MacMahon: Conceptualization, Funding acquisition, Project administration, Visualization.

Declaration of competing interest

JM is an employee of Cytokind, Inc. JM and CE are shareholders and/or option holders in Cytokind, Inc. CE is an employee and shareholder of Augmenta Bioworks, Inc. FQ is an employee of Octave Bioscience.AZO has received personal compensation for participation in scientific advisory boards, steering committees, and/or speaking engagements from Alexion Pharmaceuticals, Amgen, AstraZeneca, Banner Life Sciences, BD Biosciences, Biogen, Biologix Solutions, Bristol Myers Squibb, Celgene, EMD Serono, Genentech, GW Pharmaceuticals, Horizon Therapeutics, Jazz Pharmaceuticals, Merck, Novartis, Roche, Sandoz, Sanofi Genzyme, TG Therapeutics, and Viela Bio.

Acknowledgements

The authors wish to thank the participants of the PhoCIS study, as well as those who contributed to running the trial, biobanking of samples and conducting and analysis of the proteome assessments.

Funding: The PhoCIS trial was funded by the National Health and Medical Research Council of Australia (ID 1067209) and MS Western Australia. This project has been supported in whole or in part with federal funds from the Department of Health and Human Services; Administration for Strategic Preparedness and Response; Biomedical Advanced Research and Development Authority (BARDA), under contract number 75A50122C00064 and by Cytokind, Inc.

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