CD55 Specific Neutra™ Antibody Products

CD55, also known as decay-accelerating factor (DAF), is a glycosylphosphatidylinositol (GPI)-anchored protein that plays a critical role in protecting cells from complement-mediated damage by accelerating the decay of C3 and C5 convertases. It is involved in a variety of pathological conditions, including cancer, malaria, protein-losing enteropathy, and autoimmune diseases. CD55 deficiency can lead to complement hyperactivation, resulting in severe complications such as malabsorption and angiopathic thrombosis. Furthermore, CD55 has been identified as a host receptor for malaria and is implicated in cancer progression through mechanisms that include cell shielding, signaling pathways like JNK, JAK/STAT, MAPK/NF-κB, and promoting malignant transformation and angiogenesis. This makes CD55 a potential target for therapeutic interventions in these diseases.

Its Gene ID: 1604, UniProtKB ID: P08174, OMIM ID: 125240

The Structure of CD55

Structurally, mature CD55 is composed of three distinct domains: it includes four short consensus repeat (SCR) domains that are critical for its function in inhibiting complement activation, a serine/threonine/proline-rich region that is heavily glycosylated, and a GPI anchor that secures CD55 to the cell membrane, specifically within lipid raft microdomains. These structural features facilitate CD55's role in protecting cells from complement-mediated lysis, which is vital across various physiological and pathological contexts.

Fig.1 CD55 structure and functions in complement mediated pathway.¹

The Signal Pathway of CD55

• Tyrosine Kinase Pathways: CD55 activates LCK and FYN, non-receptor tyrosine kinases from the SRC family, crucial in cancer progression. It promotes autophosphorylation of LCK in ovarian cancer, affecting DNA repair genes and contributing to chemoresistance.
• NF-κB/MAPK Pathways: CD55 is integral in activating NF-κB and MAPK pathways in tumors, enhancing survival and growth. It transduces LPS signaling in CHO cells, triggering NF-κB translocation and MAPK phosphorylation.
• JNK Pathway: CD55 activates the JNK pathway through the LIME/ROR2 pathway in ovarian cancer, influencing the expression of pluripotency factors like SOX2, OCT4, and NANOG. This activation is pivotal for maintaining cancer stem cell properties.
• JAK/STAT3 Signaling: In ovarian cancer, CD55 activates JAK/STAT3 signaling, critical for cell survival and malignant transformation, via interaction with the CD97 receptor.
• HER2 Signaling: CD55 protects HER2-positive breast cancer cells from trastuzumab-induced complement-dependent cytotoxicity, suggesting its role in complement regulation and potential impact on therapeutic responses to HER2-targeted therapies.

Fig.2 Non-complement role of CD55 signaling in cancer.¹

Roles of CD55 in Diseases

• Malaria: CD55 acts as a crucial host receptor for Plasmodium falciparum, the parasite responsible for malaria. Loss of CD55 in erythrocytes renders them resistant to infection by preventing proper parasite adherence to the erythrocyte surface, highlighting its potential as a target for malaria therapy.
• Protein-losing Enteropathy: CD55 deficiency can lead to hyperactivation of the complement system, resulting in protein-losing enteropathy characterized by severe malabsorption and angiopathic thrombosis. This suggests that maintaining CD55 function is vital for preventing excessive complement activity that contributes to this condition.
• Paroxysmal Nocturnal Hemoglobinuria (PNH): In PNH, CD55 deficiency on erythrocytes leads to increased susceptibility to complement-mediated lysis, causing severe hemolytic anemia. CD55 is essential for protecting erythrocytes from complement attack, underscoring its therapeutic potential in managing PNH symptoms.
• Multiple Sclerosis (MS): CD55 regulates complement activation on cell surfaces, including those in the central nervous system. Its interaction with CD97 influences inflammatory processes in MS by moderating complement activity, thus playing a protective role against excessive immune responses in MS.
• Autoimmune Diseases: CD55 is implicated in various autoimmune conditions, where it modulates complement activity and reduces tissue damage. In diseases like rheumatoid arthritis, CD55's interaction with CD97 helps to regulate immune responses, suggesting a therapeutic potential for managing autoimmune pathology.

Fig.3 Roles of CD55 in diseases.²

Creative Biolabs is dedicated to offering an extensive range of services and products related to CD55 to further aid your exploration of its broad applicability and potential biological insights. Leveraging our advanced neutralizing antibody and recombinant antibody technology platform, we are capable of providing superior quality services. Our meticulously controlled and performance-verified CD55 recombinant antibody products assure reliability and efficiency in various biological research.

REFERENCES

1. Bharti, Rashmi, et al. "CD55 in cancer: Complementing functions in a non-canonical manner." Cancer Letters 551 (2022): 215935
2. Dho, So Hee, Jae Cheong Lim, and Lark Kyun Kim. "Beyond the role of CD55 as a complement component." Immune network 18.1 (2018).