CRP（C-反应蛋白）是一种由肝脏合成的急性期蛋白，属于五聚体蛋白家族（pentraxin family），该家族成员具有保守的环状五聚体结构，参与先天免疫和炎症反应。CRP的主要生物学功能是识别病原体或受损细胞表面的磷酸胆碱，通过激活补体系统（如结合C1q启动经典途径）和促进吞噬作用清除病原体或凋亡细胞。它在炎症或感染后数小时内迅速升高，是临床常用的炎症标志物。CRP的作用位点包括细菌多糖、坏死细胞膜等含有磷酸胆碱的结构，其表达受IL-6等促炎细胞因子调控。基因突变可能导致CRP水平异常，如某些单核苷酸多态性（SNPs）与基础CRP浓度相关，但严重突变罕见。CRP持续高水平与心血管疾病（如动脉粥样硬化）、自身免疫病（类风湿关节炎）和感染性疾病密切相关，其通过促进泡沫细胞形成和血管炎症加速动脉斑块发展。过表达时可能加剧慢性炎症状态或组织损伤，而基因敲除小鼠研究表明CRP缺失会削弱对细菌感染的防御能力，但对基础生理影响较小。五聚体蛋白家族还包括血清淀粉样蛋白P（SAP），它们共享钙依赖性配体结合特性和免疫调节功能，但SAP更多参与淀粉样沉积的调控。CRP的临床检测广泛用于评估炎症程度、预测心血管风险及监测治疗反应。

The CRP gene encodes C-reactive protein, an acute-phase reactant primarily synthesized by the liver that belongs to the pentraxin family, a group of proteins characterized by a conserved cyclic pentameric structure essential for innate immunity and inflammatory responses. CRP functions as a pattern recognition molecule that binds to phosphocholine residues on the surfaces of pathogens, necrotic cells, and bacterial polysaccharides, thereby facilitating the clearance of apoptotic cells and microbes. Upon binding its ligands, CRP activates the classical complement pathway by recruiting C1q and promotes opsonization to enhance phagocytosis. Its expression is tightly regulated by pro-inflammatory cytokines, particularly interleukin-6 (IL-6), leading to a rapid increase in circulating levels within hours of infection or tissue injury, which makes CRP a widely used clinical biomarker for assessing inflammation severity, monitoring therapeutic responses, and predicting cardiovascular risk. Persistent elevation of CRP is strongly associated with chronic inflammatory conditions, including atherosclerosis and autoimmune diseases such as rheumatoid arthritis, where it contributes to vascular inflammation and foam cell formation, accelerating plaque progression. While rare severe mutations can alter baseline CRP levels, common single nucleotide polymorphisms (SNPs) are often linked to variations in steady-state concentrations. Comparative studies with other pentraxins, such as serum amyloid P (SAP), highlight shared calcium-dependent ligand binding and immunomodulatory functions, although SAP is more specifically involved in amyloid deposition regulation. Experimental evidence from gene knockout mice indicates that while CRP deficiency has minimal impact on basal physiology, it significantly impairs the host's defensive capacity against bacterial infections, underscoring its critical role in the acute inflammatory response.

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