{"id":4133,"date":"2026-02-12T17:42:03","date_gmt":"2026-02-12T17:42:03","guid":{"rendered":"https:\/\/sites.manchester.ac.uk\/lydia-becker-institute\/?p=4133"},"modified":"2026-02-15T19:00:22","modified_gmt":"2026-02-15T19:00:22","slug":"refractory-myasthenia-gravis-research","status":"publish","type":"post","link":"https:\/\/sites.manchester.ac.uk\/lydia-becker-institute\/2026\/02\/12\/refractory-myasthenia-gravis-research\/","title":{"rendered":"Research identifies a distinct immune signature in treatment-resistant Myasthenia Gravis"},"content":{"rendered":"

[et_pb_section bb_built=”1″ admin_label=”section” fullwidth=”on” next_background_color=”#000000″ global_module=”322″][et_pb_fullwidth_menu global_parent=”322″ _builder_version=”3.0.106″ menu_id=”7″ submenu_direction=”downwards” fullwidth_menu=”off” background_layout=”dark” module_class=”main-navigation” \/][\/et_pb_section][et_pb_section bb_built=”1″ fullwidth=”off” specialty=”on” prev_background_color=”#000000″ next_background_color=”#1d1d1d”][et_pb_column type=”2_3″ specialty_columns=”2″][et_pb_row_inner locked=”off”][et_pb_column_inner type=”4_4″ saved_specialty_column_type=”2_3″][et_pb_post_title _builder_version=”3.0.106″ title=”on” meta=”on” author=”on” date=”on” categories=”on” comments=”on” featured_image=”on” featured_placement=”above” text_color=”dark” text_background=”off” locked=”on” parent_locked=”off” \/][et_pb_text _builder_version=”3.17.6″ background_layout=”light” parent_locked=”off”]<\/p>\n

Myasthenia Gravis (MG) is a rare autoimmune disease in which the immune system attacks the connection between nerves and muscles. This attack causes muscle weakness that can affect vision, movement, speech, swallowing, and breathing. While many patients respond to treatment, others develop a severe, treatment-resistant form of the condition known as refractory MG<\/strong>. Currently, there are no reliable biomarkers to help doctors predict which patients will respond to therapy and which will not.<\/p>\n

In a new study published in Med<\/a>, researchers aimed to uncover why these treatments fail for some individuals. To do this, the team analysed blood samples from people living with MG and compared them to those of healthy volunteers to understand the underlying cellular differences that drive standard therapy resistance.<\/p>\n

A Pattern of Immune Imbalance<\/b><\/p>\n

The study revealed distinct immune system abnormalities in patients with refractory MG. These patients showed an overactive adaptive immune response, specifically involving increased numbers of memory B cells.<\/p>\n

At the same time, the researchers found that regulatory T cells\u2014which normally act as a \u2018braking system\u2019 to suppress excessive inflammation\u2014were markedly reduced. This combination of an overactive attack and a weakened braking system contributes to significant immune dysregulation.<\/p>\n

The research also identified changes in the innate immune system, including\u00a0reduced dendritic cells<\/b>\u00a0and i<\/strong>ncreased monocytes,\u00a0<\/b>along with h<\/b>eightened activity of the complement system,\u00a0<\/b>all pointing to ongoing immune-mediated damage at the neuromuscular junction.<\/p>\n

\n

\u201cOur study identifies a distinct immune signature associated with treatment-resistant myasthenia gravis.\u00a0Understanding these immune differences brings us closer to predicting how patients will respond to therapy and to developing more targeted, personalised treatment approaches.\u201d<\/p>\n

 <\/p>\n

Dr Madhvi Menon<\/a> –\u00a0UKRI Future Leaders Fellow\u00a0<\/span>and Lead Author<\/strong><\/p>\n<\/blockquote>\n

Predicting Treatment Response<\/b><\/p>\n

The team also examined a small group of refractory patients treated with rituximab, a drug designed to remove B cells. Although B cells were successfully reduced in all patients, only some showed meaningful clinical improvement.<\/p>\n

The study found that those who did not respond appeared to have a version of the disease driven by long-lived plasma cells and particularly high complement activity. This discovery suggests that these specific patients may benefit more from therapies that target the complement pathway rather than just B cells.<\/p>\n

\u201cFor patients whose symptoms do not improve with existing treatments, the lack of clear answers can be incredibly frustrating,\u201d\u00a0said Dr Katy Dodd<\/a>, Neurology Consultant at Manchester Centre for Clinical Neuroscience.\u00a0\u201cOur findings help explain why some therapies work for certain patients but not others, and point toward more personalised approaches that could improve outcomes in the future.\u201d<\/p>\n

\u201cOur study identifies a distinct immune signature associated with treatment-resistant myasthenia gravis,” said Dr Madhvi Menon<\/a>,\u00a0UKRI Future Leaders Fellow\u00a0<\/span>at the Lydia Becker Institute of Immunology and Inflammation<\/a> and lead author of the paper. “Understanding these immune differences brings us closer to predicting how patients will respond to therapy and to developing more targeted, personalised treatment approaches.\u201d<\/p>\n