# Association of cytokine levels with treatment duration and patient family history in Egyptian multiple sclerosis patients

**Authors:** Esraa Mohsen, Hesham Haffez, Sandra Ahmed, Taghrid S. El-Mahdy, Selwan Hamed

PMC · DOI: 10.1038/s41598-026-38500-z · Scientific Reports · 2026-03-02

## TL;DR

This study examines how cytokine levels in Egyptian MS patients change with treatment duration and family history of autoimmunity.

## Contribution

The study identifies specific cytokine correlations with treatment duration and family history in Egyptian MS patients.

## Key findings

- Longer DMT treatment (>24 months) significantly reduces IL-6, TNF-α, and IFN-γ levels in MS patients.
- IL-6 correlates with worsening disability, while TNF-α is higher in patients with a family history of autoimmunity.
- IL-17A and IFN-γ show inverse correlation in treatment-naïve MS patients.

## Abstract

Multiple sclerosis (MS) is one of the diseases that is widely spreading all over the world, with no clear etiology or definite pathological mechanism. Although there is no cure for MS, multiple therapeutic agents called disease-modifying therapies (DMTs) have been developed to relieve worsening symptoms and counteract its progression. The aim of this study is to investigate the effect of DMTs on some proinflammatory cytokine levels in the serum of Egyptian MS patients over different treatment durations. Additionally, link the levels of serum cytokines with patients’ clinical parameters. A total of 192 MS Egyptian patients were recruited and classified based on treatment duration and DMT types. The levels of IL-6, IL-17A, TNF-α, and IFN-γ were detected using the ELISA technique. Results showed that MS patients treated for a period longer than 24 months were associated with a significant decrease in IL-6, TNF-α, and IFN-γ levels compared to untreated patients or patients treated for less than 12 months. IL-6 correlated directly with the Expanded Disability Status Scale score, whereas IL-17A and IFN-γ were inversely correlated in treatment-naïve MS patients. Additionally, MS patients with a family history of autoimmunity have a lower age at onset of the disease with a higher TNF-α level. In conclusion, proinflammatory cytokine levels were correlated with MS patients on long-term treatment with DMTs. IL-6 was linked with worsening disability in MS patients, while TNF-α was linked to a family history of autoimmunity.

The online version contains supplementary material available at 10.1038/s41598-026-38500-z.

## Linked entities

- **Proteins:** IL6 (interleukin 6), IL17A (interleukin 17A), TNF (tumor necrosis factor), IFNG (interferon gamma)
- **Diseases:** multiple sclerosis (MONDO:0005301)

## Full-text entities

- **Genes:** IL17RA (interleukin 17 receptor A) [NCBI Gene 23765] {aka CANDF5, CD217, CDw217, IL-17RA, IL17R, IMD51}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CSF2 (colony stimulating factor 2) [NCBI Gene 1437] {aka CSF, GMCSF}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}, CCR6 (C-C motif chemokine receptor 6) [NCBI Gene 1235] {aka BN-1, C-C CKR-6, CC-CKR-6, CCR-6, CD196, CKR-L3}, LTA (lymphotoxin alpha) [NCBI Gene 4049] {aka LT, TNFB, TNFSF1, TNLG1E}, IFNB1 (interferon beta 1) [NCBI Gene 3456] {aka IFB, IFF, IFN-beta, IFNB}, POLI (DNA polymerase iota) [NCBI Gene 11201] {aka RAD30B, RAD3OB, eta2}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CXCR3 (C-X-C motif chemokine receptor 3) [NCBI Gene 2833] {aka CD182, CD183, CKR-L2, CMKAR3, GPR9, IP10-R}, CD36 (CD36 molecule (CD36 blood group)) [NCBI Gene 948] {aka BDPLT10, CHDS7, FAT, GP3B, GP4, GPIV}, HLA-DRB1 (major histocompatibility complex, class II, DR beta 1) [NCBI Gene 3123] {aka DRB1, HLA-DR1B, HLA-DRB, SS1}, GP2 (glycoprotein 2) [NCBI Gene 2813] {aka ZAP75}, HLA-B (major histocompatibility complex, class I, B) [NCBI Gene 3106] {aka AS, B-4901, HLAB}
- **Diseases:** ataxia (MESH:D001259), demyelinating disease (MESH:D003711), brain lesions (MESH:D001927), RA (MESH:D001172), gliosis (MESH:D005911), CVS (MESH:D012170), Relapsing remitting multiple sclerosis (MESH:D020529), DMT (MESH:D016609), infections (MESH:D007239), EAE (MESH:D004681), degeneration (MESH:D009410), NMO (MESH:D009471), -remitting (MESH:C535355), CDMS (MESH:D009103), loss (MESH:D016388), immunoinflammatory diseases (MESH:D004194), inflammation (MESH:D007249), limb weakness (MESH:D018908), sensory abnormalities (MESH:D012678), psychiatric symptoms (MESH:D001523), paralysis (MESH:D010243), autoimmune disease (MESH:D001327), lesions (MESH:D009059), hemolysis (MESH:D006461), SLE (MESH:D008180)
- **Chemicals:** Fingolimod (MESH:D000068876), ocrelizumab (MESH:C533411), DMT (-), Rituximab (MESH:D000069283), natalizumab (MESH:D000069442), teriflunomide (MESH:C527525), DMF (MESH:D000069462), fumarates (MESH:D005650), alemtuzumab (MESH:D000074323), vitamin D (MESH:D014807), glatiramer acetate (MESH:D000068717), iron (MESH:D007501), methotrexate (MESH:D008727)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

13 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957492/full.md

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Source: https://tomesphere.com/paper/PMC12957492