| Psoriasis |
Dendritic cells, Th17/Th1 cells, keratinocytes, neutrophils |
IL-23/IL-17 axis → keratinocyte hyperproliferation; TNF signaling |
Well-demarcated scaly erythematous plaques (skin) |
Topical steroids, phototherapy, methotrexate/cyclosporine; biologics (anti-TNF, anti-IL-17, anti-IL-23) |
| Multiple Sclerosis (MS) |
Autoreactive CD4 (Th1/Th17), CD8 T cells, B cells, microglia, macrophages |
Autoimmune demyelination in CNS; blood–brain barrier breach; complement & cytotoxicity |
Relapses of focal neuro deficits, sensory/motor impairment, visual problems |
High-dose corticosteroids (relapses), disease-modifying therapies: interferon-β, S1P modulators, anti-CD20 (rituximab/ocrelizumab), natalizumab |
| Crohn’s Disease |
Innate immune cells, Th1/Th17, B cells, macrophages |
Barrier dysfunction, dysregulated mucosal immunity (NOD2, IL-12/23, TNF); chronic transmural inflammation |
Abdominal pain, diarrhea, weight loss, fistulas |
Aminosalicylates (limited), corticosteroids (induction), immunomodulators (azathioprine), anti-TNF, anti-IL-12/23 |
| HIV → AIDS |
CD4⁺ T cells (primary target), macrophages, dendritic cells |
Lentiviral infection → progressive CD4 depletion, immune deficiency, opportunistic infections |
Lymphadenopathy → opportunistic infections, weight loss, chronic fever |
Combination antiretroviral therapy (ART); opportunistic infection prophylaxis |
| SLE (systemic lupus erythematosus) |
B cells, plasmablasts, Tfh, plasmacytoid DCs, complement |
Autoantibodies (anti-dsDNA), immune complexes → complement activation; type I IFN signature |
Malar rash, arthritis, nephritis, cytopenias, photosensitivity |
Hydroxychloroquine, corticosteroids, immunosuppressants (azathioprine, mycophenolate), biologics (belimumab), supportive care |
| Aicardi–Goutières Syndrome (AGS) |
Microglia, innate immune sensors, plasmacytoid DCs |
Genetic defects in nucleic acid metabolism → chronic type I interferonopathy (sensing of self-nucleic acids) |
Early onset encephalopathy, intracranial calcifications, developmental delay |
Supportive; immunomodulation (JAK inhibitors) and symptomatic care (experimental) |
| COPA syndrome |
T cells, B cells, innate immune cells |
Defect in ER-Golgi transport → autoimmune/autoinflammatory phenotype often with elevated type I IFN |
Interstitial lung disease, arthritis, autoimmunity |
Immunosuppression (steroids, calcineurin inhibitors), targeted approaches (JAK inhibitors); lung transplant in severe ILD |
| Alzheimer’s disease (microglia-related aspects) |
Microglia, complement components, astrocytes |
Microglial activation, complement-mediated synapse pruning, TREM2 pathway; chronic neuroinflammation |
Progressive memory loss, cognitive decline |
Symptomatic drugs (AChE inhibitors, memantine); anti-amyloid / anti-tau immunotherapies (experimental); symptomatic/supportive care |
| Autism Spectrum Disorder (ASD) — microglia associations |
Microglia (proposed role), peripheral immune cells (associations) |
Associations of neuroimmune dysregulation in some cases (microglial activation/inflammation) — heterogeneous and incompletely understood |
Social-communication deficits, restricted/repetitive behaviors |
Behavioral therapies (ABA), developmental interventions; no standard immunotherapy (research ongoing) |
| Sepsis |
Innate immune cells (neutrophils, macrophages), endothelial cells, lymphocytes |
Dysregulated host response to infection → excessive cytokines, coagulopathy, immune paralysis/sequential hypo-inflammation |
Fever/hypothermia, tachycardia, hypotension, organ dysfunction |
Early antibiotics, source control, fluid resuscitation, vasopressors, organ support; adjunctive immunomodulation selective in trials |
| COVID-19 (severe) |
Epithelial cells, innate immune cells, T cells, neutrophils |
Viral infection with possible hyperinflammation (cytokine storm), coagulopathy, impaired antiviral immunity |
Fever, cough, dyspnea → hypoxemia, ARDS in severe cases |
Antivirals (where approved), dexamethasone for severe disease, supportive care, monoclonal antibodies (prophylaxis/early disease), vaccines (preventive) |
| Rheumatic Fever |
Cross-reactive T/B cells, antibodies |
Molecular mimicry after Group A strep → immune cross-reaction against heart/striatum → carditis |
Fever, migratory polyarthritis, carditis, chorea (Sydenham) |
Eradicate streptococcal infection (penicillin), anti-inflammatory therapy (aspirin, steroids), long-term prophylaxis |
| Rheumatoid Arthritis (RA) |
Synovial macrophages, fibroblast-like synoviocytes, Th17, B cells (autoantibodies RF/ACPA) |
Autoantibody-associated chronic synovitis; TNF, IL-6, IL-1 pathways; joint erosion mediated by osteoclasts |
Symmetric peripheral polyarthritis, morning stiffness, joint erosions |
NSAIDs, glucocorticoids (bridging), DMARDs (methotrexate), biologics (anti-TNF, anti-IL-6, anti-CD20) |
| Rheumatic Heart Disease (RHD) |
Result of post-streptococcal immune injury (T/B cells) |
Chronic valvular damage from immune cross-reactivity after rheumatic fever |
Valvular regurgitation/stenosis, heart failure, arrhythmias |
Secondary prophylaxis (penicillin), medical management of heart failure; valve repair/replacement surgery |
| Guillain–Barré syndrome (GBS) |
Peripheral nerve-targeting antibodies, complement, macrophages |
Autoimmune peripheral demyelination (often post-infection); anti-ganglioside antibodies in subtypes → complement & macrophage-mediated injury |
Rapidly progressive ascending weakness, areflexia, possible respiratory failure |
IV immunoglobulin (IVIG) or plasmapheresis, supportive respiratory care, rehab |
| Cancer (immune aspects) |
Cytotoxic CD8 T cells, NK cells, tumor-associated macrophages, Tregs, MDSCs |
Immune evasion (PD-L1, CTLA-4, antigen loss), chronic inflammation, immunosuppressive tumor microenvironment |
Variable by tumor type — mass effect, organ-specific symptoms, constitutional symptoms |
Surgery, chemo, radiotherapy; immunotherapies: checkpoint inhibitors (anti-PD-1/PD-L1, anti-CTLA-4), CAR-T, cytokine therapies, targeted small molecules |