Sjögren’s Disease Isn’t One-Size-Fits-All—And Science Is Finally Catching Up

 

If you’ve been diagnosed with Sjögren’s disease (SjD), you already know it’s not just about dry eyes and fatigue. It’s a complex autoimmune condition that can affect your entire body—from your salivary glands to your lungs, skin, and even your risk for lymphoma.

But here’s the thing: not all Sjögren’s is the same. And a new study is helping us understand why.

The Study That’s Changing the Game

Researchers recently used single-cell and spatial transcriptomics—basically, ultra-detailed molecular mapping—to compare two major subtypes of Sjögren’s:

• Anti-SSA-positive SjD (the more common type, often with systemic symptoms)

• Anti-centromere-positive SjD (less common, often overlaps with systemic sclerosis)

They also looked at patients who were double-positive and those with seronegative SjD (Sicca).

Their goal? To uncover what’s happening at the cellular level in the salivary glands—and how different autoantibodies might shape the disease.

What They Found

1. Your Antibodies Tell a Story

• SSA-positive patients had higher levels of inflammation and immune activation, especially involving interferon (IFN) pathways—a hallmark of more aggressive autoimmune activity.

• CENT-positive patients showed signs of fibrosis (scarring) and had immune profiles that resembled systemic sclerosis, including symptoms like Raynaud’s and skin tightening.

2. Your Immune System Is Overactive

In Sjögren’s, two types of immune cells—T cells and B cells—are doing too much.

• T cells are like the body’s security guards. In some people, they attack healthy tissue by mistake.

• B cells make antibodies. In Sjögren’s, they make ones that target your own body, keeping inflammation going.

Different types of Sjögren’s have different mixes of these cells, which helps explain why symptoms can vary from person to person.

• Across all SjD types, researchers found activated T cells and B cells in the salivary glands.

• SSA-positive patients had more CD8+ T cells (which can directly kill tissue), while CENT-positive patients leaned toward CD4+ T cells (which coordinate immune responses).

• B cells weren’t just hanging around—they were actively responding to disease-specific antigens, meaning they were part of the problem, not just bystanders.

3. Fibroblasts Are More Than Just Support Cells

• Fibroblasts—those structural cells in your tissues—were found to play a major role in sustaining inflammation.

• They help build tertiary lymphoid structures, which are like mini immune hubs that keep the attack going.

Why This Matters to You

This research shows that Sjögren’s isn’t a single disease—it’s a spectrum, shaped by your unique antibody profile. That means:

• Diagnosis could become more precise, especially for CENT-positive patients who are often misclassified as “seronegative.”

• Targeted treatments could be developed based on your molecular subtype.

• Fibroblasts might become a new treatment target, especially for those with fibrosis or chronic inflammation.

What You Can Do Now

While this research is still in early stages, it’s a powerful reminder that your symptoms—and your biology—matter. Here’s how to stay empowered:

• Ask your doctor about your antibody profile (SSA, SSB, CENT, etc.)

• Track your symptoms and note any systemic features like skin changes or Raynaud’s

• Stay informed—science is moving fast, and personalized medicine is on the horizon

• Connect with others—support groups and advocacy communities can help you navigate the journey

• Read the original study published in September 2025