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Emerging Biologic Therapies in Autoimmune Diseases: Focus on
Pemphigus Vulgaris, Generalized Myasthenia Gravis, and Psoriasis
Asha Nandabaram*, Poojitha Kalvala, Lakshmi Manisha Rajaputana, Bhavani Bachu, Muvvala
Sudhakar
Department of Pharmacology, Malla Reddy College of Pharmacy, Affiliated to Osmania University,
Hyderabad, India.
Corresponding Author*
DOI: https://doi.org/10.51244/IJRSI.2025.120800197
Received: 04 Sept 2025; Accepted: 10 Sept 2025; Published: 19 September 2025
ABSTRACT
Biologic therapies have transformed the management of autoimmune diseases by targeting key immune
pathways with precision, reducing dependence on broad immunosuppression. This review explores advances
in monoclonal antibody–based therapies across three representative autoimmune conditions: pemphigus
vulgaris (PV), generalized myasthenia gravis (gMG), and psoriasis. In PV, B-cell depletion with rituximab has
become the preferred first-line therapy, achieving durable remission and steroid-sparing outcomes. In gMG,
complement inhibitors (eculizumab, ravulizumab, zilucoplan) and neonatal Fc receptor (FcRn) antagonists
(efgartigimod, rozanolixizumab) provide rapid, clinically meaningful improvements in refractory patients. In
psoriasis, therapies targeting the IL-23/IL-17 axis (guselkumab, risankizumab, bimekizumab) have achieved
unprecedented levels of skin clearance and durability. Safety, accessibility, and biomarker-driven
personalization remain challenges, while future directions include antigen-specific cell therapies, bispecific
antibodies, and oral biologic mimetics. Collectively, these advances highlight the transformative role of
biologics in autoimmune disease and the trajectory toward precision immunotherapy.
Keywords: Biologics, Monoclonal antibodies, Pemphigus vulgaris, Myasthenia gravis, Psoriasis, Autoimmune
diseases, FcRn inhibitors, IL-23 inhibitors
INTRODUCTION
Monoclonal antibodies and biologic therapies have revolutionized the management of autoimmune diseases by
enabling targeted immunomodulation rather than broad immunosuppression. These agents exploit diverse
immune pathways, including cytokine-directed strategies (e.g., TNF-α and interleukin blockade), B-cell–
directed depletion, integrin inhibition, and co-stimulation modulation [1]. The development of monoclonal
antibodies and fusion proteins has transformed immunotherapy by allowing precise targeting of immune cell
receptors and cytokines [1]. Contemporary approaches can be categorized into those that globally suppress
immune responses versus those that promote “operational tolerance” — selectively attenuating pathogenic
autoimmune responses while sparing protective immunity. Among these, TNF-α inhibitors and CD20-directed
therapies represent landmark examples [1]. Such advances have demonstrated remarkable progress across
conditions including rheumatoid arthritis, psoriasis, inflammatory bowel disease, ankylosing spondylitis, and
juvenile idiopathic arthritis [1].
Building on this broad impact, monoclonal antibodies have also transformed outcomes in rare but severe
autoimmune diseases that were historically difficult to manage. In pemphigus vulgaris (PV), B-cell–directed
therapy with rituximab has emerged as a first-line standard, demonstrating superior remission rates and
steroid-sparing effects compared with conventional immunosuppressants [4]. In generalized myasthenia gravis
(gMG), biologics targeting the complement pathway (eculizumab, ravulizumab, zilucoplan) or blocking FcRn-
mediated IgG recycling (efgartigimod, rozanolixizumab) have reshaped treatment algorithms for refractory
disease [8–13]. In psoriasis, biologics targeting the IL-17 and IL-23 axes (bimekizumab, guselkumab,
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risankizumab) have set new efficacy benchmarks, achieving durable skin clearance with favourable safety [14–
20]. Collectively, these examples illustrate the paradigm shift from generalized immunosuppression to
precision immunotherapy tailored to specific immune mechanisms.
Pemphigus Vulgaris (PV)
Pathogenesis and Rationale
Pemphigus vulgaris (PV) is a rare but potentially life-threatening autoimmune blistering disease in which IgG
autoantibodies target desmoglein-1 and desmoglein-3, disrupting keratinocyte adhesion and leading to
acantholysis and mucocutaneous blistering. Traditional therapy has relied on high-dose corticosteroids and
broad immunosuppressants (azathioprine, cyclophosphamide, mycophenolate mofetil), which reduce disease
activity but are associated with substantial morbidity, including opportunistic infections, osteoporosis,
metabolic complications, and increased mortality. The recognition of B cells as central drivers of PV
pathogenesis provided the rationale for B-cell–directed biologics as disease-modifying agents.
Rituximab as a Paradigm Shift
Rituximab, a chimeric anti-CD20 monoclonal antibody, represented the first major breakthrough. Early case
series and observational studies suggested efficacy in inducing long-term remission. The pivotal PEMPHiX
trial [4] provided high-level evidence by comparing rituximab with mycophenolate mofetil in patients with
moderate-to-severe PV. Rituximab achieved sustained complete remission in 40% of patients at 52 weeks
versus only 10% with MMF, while also enabling significant corticosteroid sparing. These findings firmly
established rituximab as first-line therapy for PV.
Further support came from the Ritux 3 regimen [5], which demonstrated that early introduction of rituximab
plus short-course corticosteroids resulted in long-lasting remission, with many patients remaining steroid-free
for years. These results highlight how biologics have transformed PV management from chronic steroid
dependence to durable, targeted disease control.
Safety Profile
Rituximab is generally well tolerated. The most common adverse events are infusion reactions and mild
infections. Rare but serious risks include hepatitis B reactivation and progressive multifocal
leukoencephalopathy (PML), underscoring the need for screening and pharmacovigilance. Long-term follow-
up studies indicate that repeat courses remain safe and effective, with no major cumulative toxicity reported.
Emerging Therapies
The limitations of rituximab—delayed onset and incomplete remission in some patients—have prompted
exploration of novel therapies. Rilzabrutinib, a Bruton’s tyrosine kinase (BTK) inhibitor, demonstrated
encouraging efficacy in phase 2 trials, but the PEGASUS phase 3 study failed to meet its primary endpoint,
highlighting challenges in translating preclinical success to robust clinical outcomes. Other promising
investigational strategies include desmoglein-specific CAR-T cell therapy (DSG3-CAART), which seeks to
selectively eliminate autoreactive B cells, and next-generation anti-CD20 mAbs (ocrelizumab, ofatumumab)
with potentially improved safety profiles.
Table 1: Key Biologic Therapies in Pemphigus Vulgaris (PV)
Agent
Target
Pivotal Trial(s)
Population /
Endpoints
Safety Profile
Rituximab
CD20 B
cells
PEMPHiX
(NEJM 2021)
Moderate–
severe PV,
rituximab vs
Infusion
reactions, viral
reactivation
(HBV), rare
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MMF
PML
Rituximab
(Ritux 3
regimen)
CD20 B
cells
JAMA Derm
2024
Newly
diagnosed PV
Similar to above;
generally well
tolerated with
repeat dosing
Rilzabrutinib
BTK
PEGASUS
Phase 3 (2022)
Moderate–
severe PV
Headache, GI
symptoms; no
major safety
signals
Emerging:
DSG3-CAART
/ CAR-T
Autoantigen-
specific
RESET-PV
(early phase)
Refractory PV
Still under
investigation
Rituximab has fundamentally changed the treatment paradigm in PV, shifting care toward targeted, B-cell–
directed immunotherapy that offers durable remission with reduced steroid exposure. The future lies in refining
therapies to further enhance specificity and safety.
Generalized Myasthenia Gravis (gMG)
Pathogenesis and Rationale
Generalized myasthenia gravis (gMG) is an autoimmune neuromuscular disorder primarily caused by
autoantibodies against the acetylcholine receptor (AChR), though some patients harbor antibodies against
muscle-specific kinase (MuSK) or other antigens. These antibodies impair neuromuscular transmission,
producing fatigable muscle weakness. Standard therapies—acetylcholinesterase inhibitors, corticosteroids, and
immunosuppressants—provide partial and often nonspecific control. Advances in immunology identified
complement activation and pathogenic IgG persistence as central mechanisms, leading to the development of
biologics targeting these pathways.
Complement Inhibitors
Eculizumab [8]: This terminal complement (C5) inhibitor demonstrated significant improvements in
MG-ADL and QMG scores in refractory AChR+ gMG patients. Benefits appeared within weeks and
were sustained with long-term therapy. However, the need for IV infusions every 2 weeks and the risk
of meningococcal infection limited practicality.
Ravulizumab [10]: A long-acting derivative of eculizumab, ravulizumab offers comparable efficacy
with infusions every 8 weeks, greatly improving convenience. Its efficacy was consistent across
subgroups, making it an attractive alternative.
Zilucoplan [13]: A novel subcutaneous peptide inhibitor of C5, zilucoplan provides at-home dosing
with robust improvements in MG-ADL and QMG, further broadening the complement blockade
armamentarium.
FcRn Inhibitors
The neonatal Fc receptor (FcRn) regulates IgG recycling, prolonging the half-life of pathogenic antibodies. Its
inhibition accelerates IgG degradation, reducing autoantibody burden.
Efgartigimod [11]: An engineered Fc fragment antagonist, efgartigimod produced rapid, clinically
meaningful improvements in MG-ADL, with individualized treatment cycles tailored to patient
response.
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Rozanolixizumab [12]: Administered subcutaneously, rozanolixizumab demonstrated significant
improvements in MG-ADL and QMG in both AChR+ and MuSK+ patients, highlighting broad
applicability.
Safety Profile
Complement inhibitors carry an increased risk of meningococcal infections, requiring vaccination and
prophylaxis, while FcRn inhibitors are generally well tolerated, with headache and gastrointestinal symptoms
most frequently reported.
Emerging Therapies
Other FcRn inhibitors (e.g., nipocalimab) and additional complement modulators are in late-phase
development. B-cell–targeted therapy with rituximab shows clear benefit in MuSK+ MG, though results are
inconsistent in AChR+ disease.
Table 2: Key Biologic Therapies in Generalized myasthenia gravis (gMG)
Agent
Target
Pivotal
Trial(s)
Population /
Endpoints
Key Efficacy Results
Safety Profile
Eculizumab
C5
complement
REGAIN
(NEJM 2017)
AChR+
refractory
gMG
Significant
improvement in MG-
ADL/QMG; rapid
onset (weeks)
Meningococcal
infection risk;
requires
vaccination
Ravulizumab
C5
complement
(long-acting)
CHAMPION-
MG (2022)
AChR+ gMG
Non-inferior to
eculizumab; q8-week
dosing; durable benefit
Similar to
eculizumab;
fewer infusions
Zilucoplan
C5 peptide
inhibitor
(SC)
RAISE
(Lancet
Neurol 2023)
AChR+ gMG
Significant MG-
ADL/QMG
improvement;
convenient SC dosing
Injection site
reactions;
generally well
tolerated
Efgartigimod
FcRn
antagonist
ADAPT
(Lancet 2021)
AChR+ gMG
Rapid MG-ADL/QMG
improvement;
individualized cycles
Headache, mild
infections;
favorable safety
Rozanolixizumab
FcRn
antagonist
(SC)
MycarinG
(Lancet
Neurol 2023)
AChR+ and
MuSK+ gMG
Significant MG-
ADL/QMG
improvement; weekly
SC dosing
Nausea,
headache;
generally well
tolerated
Rituximab (off-
label)
CD20 B cells
Mixed trials /
MuSK+ MG
MuSK+ MG,
refractory
cases
Effective in MuSK+
subtype; inconsistent
AChR+ results
Infusion
reactions,
infections
The approval of complement and FcRn inhibitors has ushered in a new era of gMG management, enabling
rapid, targeted, and durable symptom control while reducing dependence on broad immunosuppressants.
Psoriasis
Pathogenesis and Rationale
Psoriasis is a chronic, immune-mediated inflammatory disease of the skin, recognized globally as a serious
non-communicable condition by the WHO due to its prevalence, morbidity, and psychosocial burden. Beyond
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skin manifestations, psoriasis is strongly associated with comorbidities such as psoriatic arthritis,
cardiovascular disease, psychiatric disorders, and liver disease. Genetic predisposition is a major determinant,
with over 60 susceptibility loci identified by genome-wide association studies and the HLA-Cw6 allele being
particularly linked to early-onset disease.
Immunopathogenesis centers on dysregulated Th17 and Th22 responses, with cytokines such as IL-17, IL-22,
IL-23, and TNF-α driving keratinocyte proliferation and chronic inflammation. Interactions between dendritic
cells, antimicrobial peptides, and keratinocytes form a feedback loop that sustains disease activity. Clinically,
psoriasis is heterogeneous, with multiple subtypes including plaque psoriasis, guttate, pustular, erythrodermic,
scalp, nail, and palmoplantar psoriasis. This variability influences both disease burden and therapeutic
selection.
Treatment Evolution
Traditional systemic therapies—methotrexate, cyclosporine, and acitretin—remain effective for moderate to
severe psoriasis but are limited by toxicity and long-term tolerability. Phototherapy, including narrow-band
UVB and PUVA, is a valuable adjunct for selected patients. The introduction of biologics targeting IL-17
(secukinumab, ixekizumab) and IL-12/23 (ustekinumab) represented a breakthrough, offering targeted
immunomodulation with favourable efficacy and safety profiles. More recently, JAK inhibitors and
personalized medicine approaches have emerged as promising strategies, emphasizing individualized care and
integration of lifestyle modifications, patient education, and stress management into treatment planning.
Herbal and Natural Approaches
Alongside biologic therapies, recent research has highlighted the potential of natural products in psoriasis
management. For instance, a 2024 study evaluated ointments containing hydro-alcoholic leaf extract of Cassia
auriculata and demonstrated favourable physical properties, stability, and non-irritant profiles, supporting its
traditional use in inflammatory skin disorders. The authors concluded that Cassia auriculata ointment may
represent a promising adjunctive or alternative approach in psoriasis treatment. Such findings underscore the
importance of integrating traditional medicinal plants into modern therapeutic frameworks, particularly in
regions where access to biologics is limited. [30]
IL-17 and IL-23 Pathway Inhibitors
Bimekizumab [17,18]: As a dual IL-17A/F inhibitor, bimekizumab demonstrated superior PASI 90/100
responses compared to adalimumab and secukinumab, setting new benchmarks for efficacy. Oral
candidiasis was more frequent but typically mild and manageable.
Guselkumab [15]: An IL-23 p19 inhibitor, guselkumab proved superior to secukinumab at week 48 for
PASI 90, with highly durable responses.
Risankizumab [14]: Another IL-23 inhibitor, risankizumab achieved significantly higher PASI 90/100
rates than ustekinumab, with convenient q12-week dosing.
Tildrakizumab [20]: Showed long-term efficacy with favorable safety and drug survival rates.
Safety Profile
IL-23 inhibitors are among the safest biologics in dermatology, with low infection risk and excellent
tolerability. IL-17 inhibitors are associated with candidiasis and mild respiratory infections, but serious adverse
events remain rare.
Emerging Therapies
Next-generation therapies include oral IL-23 pathway inhibitors (e.g., icotrokinra/JNJ-2113), which aim to
combine the efficacy of biologics with the convenience of oral dosing.
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Table 3: Key Biologic Therapies in Psoriasis
Agent
Target
Pivotal Trial(s)
Population /
Endpoints
Key Efficacy Results
Safety Profile
Bimekizumab
IL-17A/F
BE SURE, BE
RADIANT
(NEJM 2021)
Moderate–
severe plaque
psoriasis
PASI 90/100 rates
superior to adalimumab
and secukinumab
Oral candidiasis
(10–15%),
mild/moderate
Guselkumab
IL-23 p19
ECLIPSE
(Lancet 2019)
Moderate–
severe psoriasis
PASI 90 at week 48
superior to secukinumab
Favorable; low
infection risk
Risankizumab
IL-23 p19
UltIMMa-1/2
(Lancet 2018)
Moderate–
severe psoriasis
PASI 90: ~75% vs 47%
(ustekinumab); durable
q12w dosing
Favorable;
minimal
immunogenicity
Tildrakizumab
IL-23 p19
reSURFACE
trials (2017)
Moderate–
severe psoriasis
Sustained PASI 75/90
clearance long-term
Good safety; low
discontinuation
rates
Secukinumab
IL-17A
ERASURE,
FIXTURE
(2014)
Moderate–
severe psoriasis
PASI 75/90 high rates at
12–16 wks; rapid onset
Nasopharyngitis,
candidiasis risk
Ixekizumab
IL-17A
UNCOVER
trials (2016)
Moderate–
severe psoriasis
High PASI 90/100 rates
at 12–16 wks; durable
Candidiasis, mild
infections
Psoriasis has become a model for precision biologic therapy, with IL-23 and dual IL-17 inhibitors delivering
high-level clearance, durable remission, and favorable safety, reshaping long-term disease expectations.
DISCUSSION AND CONCLUSION
The emergence of monoclonal antibodies and biologic therapies has redefined the therapeutic landscape of
autoimmune diseases, offering precision immunomodulation where broad immunosuppression once
dominated. Across diverse conditions such as pemphigus vulgaris, generalized myasthenia gravis, and
psoriasis, biologics have proven transformative by targeting disease-specific pathogenic pathways while
sparing global immune function.
In pemphigus vulgaris, B-cell depletion with rituximab has shifted the standard of care from long-term
corticosteroid dependency to durable remission, highlighting the central role of autoreactive B cells in disease
propagation. The success of rituximab underscores the broader principle that selective elimination of immune
effector populations can achieve lasting disease control, a concept echoed in other autoantibody-driven
conditions.
In generalized myasthenia gravis, mechanistic insights into complement activation and IgG recycling enabled
the development of complement inhibitors (eculizumab, ravulizumab, zilucoplan) and FcRn antagonists
(efgartigimod, rozanolixizumab). These therapies provide rapid and sustained symptom relief with tailored
dosing regimens, illustrating how biologics can directly modulate disease physiology to deliver meaningful
functional improvements in previously refractory patients.
In psoriasis, advances in understanding the IL-23/Th17 axis transformed management from partial clearance
with TNF inhibitors to near-complete skin clearance with IL-17 and IL-23 inhibitors. Psoriasis thus serves as a
model of how pathway-specific targeting can achieve outcomes once thought unattainable, including long-term
disease control with high safety margins.
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Despite these successes, challenges remain. Safety considerations—ranging from infusion reactions and
opportunistic infections (PV, gMG) to candidiasis with IL-17 blockade (psoriasis)—necessitate vigilant
monitoring. Cost and access are major barriers, particularly in low- and middle-income regions, limiting the
global impact of these therapies. Furthermore, the need for biomarkers to predict response and guide patient
selection remains unmet across all three diseases.
Looking forward, the trajectory of biologic development points toward next-generation strategies: antigen-
specific cell therapies (DSG3-CAART in PV), oral biologic mimetics (e.g., IL-23 inhibitors in psoriasis), and
novel complement or FcRn modulators in gMG. These innovations promise to refine efficacy, safety, and
convenience, while the eventual integration of precision medicine approaches may enable personalized therapy
aligned to individual immune signatures.
Collectively, the experiences from pemphigus vulgaris, generalized myasthenia gravis, and psoriasis illustrate
the transformative potential of biologic therapies in autoimmune disease. By shifting paradigms from broad
immunosuppression to targeted precision immunotherapy, biologics not only improve patient outcomes but
also provide a blueprint for future therapeutic innovation across the autoimmune spectrum.
Future Perspectives
The remarkable success of biologic therapies in pemphigus vulgaris, generalized myasthenia gravis, and
psoriasis reflects not only advances in immunology but also the ongoing refinement of biotechnology
platforms. As these fields mature, several themes are shaping the next generation of autoimmune therapeutics.
1. Antigen-Specific Cell Therapies
While broad B-cell depletion with rituximab has been highly effective in PV, it is inherently nonspecific.
Antigen-targeted approaches such as chimeric autoantibody receptor T cells (CAAR-T) are in early
development. DSG3-CAART, for example, aims to selectively eliminate B cells producing pathogenic
desmoglein antibodies while sparing protective immunity. Early studies suggest feasibility, though
optimization of safety and durability will be critical before clinical adoption.
2. Next-Generation FcRn and Complement Modulators
In gMG, FcRn inhibition and complement blockade have proven transformative. Future therapies may offer
oral FcRn inhibitors or subcutaneous long-acting complement blockers, improving convenience and
adherence. Additionally, bispecific antibodies targeting both complement and FcRn pathways simultaneously
could theoretically provide deeper disease control with fewer injections.
3. Oral Biologic Mimetics
In psoriasis, biologics have set unprecedented efficacy standards, but their parenteral administration remains a
barrier. Novel oral peptide agents such as icotrokinra (JNJ-2113), designed to inhibit the IL-23/IL-17 pathway,
are demonstrating high levels of skin clearance in early trials, rivaling injectable biologics. If validated, these
agents could democratize access and adherence, particularly in resource-limited settings.
4. Bispecific and Multispecific Antibodies
The next wave of monoclonal antibody engineering includes bispecific antibodies capable of targeting two
immune pathways simultaneously (e.g., IL-17 + IL-23 dual blockade). Such strategies may provide synergistic
efficacy, reduced immunogenicity, and simplified regimens compared with combination therapy.
5. Precision Medicine and Biomarkers
Despite high efficacy rates, not all patients respond equally to biologics. The integration of biomarkers of
immune signatures (autoantibody profiles, cytokine networks, genetic susceptibility) may guide treatment
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selection and predict response, enabling a truly personalized approach. In the future, treatment may be
individualized not only by disease but also by patient-specific immune phenotypes.
6. Access, Cost, and Sustainability
Perhaps the most pressing future challenge is ensuring equitable access. Biosimilars of rituximab and TNF
inhibitors have already improved affordability in some regions. The expansion of biosimilars for IL-17 and IL-
23 inhibitors, alongside novel oral small molecules, may help balance innovation with global accessibility.
In summary, future directions in biologic therapy are defined by a dual focus: greater precision (antigen-
specific or multispecific targeting) and greater accessibility (oral mimetics, biosimilars). Together, these
advances promise to consolidate the biologic revolution while making it more patient-centered, sustainable,
and globally impactful.
Conflict of Interest: The authors declare no conflict of interest.
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