Rheumatoid arthritis is a chronic, inflammatory, systemic autoimmune disease that manifests as persistent and progressive synovitis of the peripheral joints, followed by cartilage destruction and bone destruction, resulting in joint deformity. Early rheumatoid arthritis patients are patients with rheumatoid arthritis with a disease duration of less than 1 year, in accordance with the American Rheumatism Association (AKA) 1987 classification criteria, compared with typical RA patients, early RA patients have the following characteristics: insidious and variable symptoms, relying only on clinical manifestations of diagnosis is difficult; rheumatoid factor (RF) low variability, poor diagnostic specificity; rapid disease progression In the first year, bone destruction is the fastest progress, but in the X-ray found joint destruction and can not be set as an early diagnosis, there are statistics, early RA from the appearance of symptoms to confirm the diagnosis of the time an average of 36 weeks, often missed the best time for treatment. 1, anti-keratin layer antibody (AKA) anti-keratin layer antibody was detected in the serum of rheumatoid arthritis (RA) by Young in 1979 using indirect immunofluorescence (IIF), using the epithelium of the middle 1/3 segment of the rat esophagus as a substrate, and found to be highly specific for RA, which has attracted widespread attention. This antibody specifically binds to the rat esophageal epithelial stratum corneum (SC) and is often referred to as AKA (Anti-Keratin Antibodies). In the past, most scholars did not compare, analyze and type the various types of fluorescence patterns when performing AKA assays, but rather vaguely used the appearance of linear or laminar fluorescence in the esophageal epithelial stratum corneum as a positive criterion, which is not exactly what it means. In 1989, Vincent et al. suggested that only when the stratum corneum showed strong linear or lamellar fluorescence and the stratum spinosum did not show weak fluorescence or had weak fluorescence, it could be considered as an antibody specific for RA. The nature of the murine esophageal SC antigen that binds specifically to AKA has been largely clarified. Therefore, the corresponding antibodies to the antigen should be called anti-keratin antibodies or anti-keratin antibodies keratin type. AKA is mainly IgG type, but IgM type is also seen, but has no clinical value. The average diagnostic sensitivity of IgG AKA for RA is greater than 46% and the average specificity is close to 98%, so it is considered to be the most specific biological criterion for RA. before the manifestation of clinical symptoms. It is particularly useful in patients with RA who are difficult to distinguish from other joint diseases in the early stages, and IgG AKA correlates with the severity and disease activity of RA, but not with the duration of the disease. The higher the serum titer, the greater the diagnostic value, and Youinou et al. reported that a titer of 1:40 or higher is diagnostic. the presence of AKA not only helps in the diagnosis of RA, but also allows for dynamic detection of changes in serum AKA titer to estimate disease activity and prognosis. In 1964, Dutch scholars Nieenhuis and Mandema used human buccal mucosal epithelial cells as antigen substrate for the first time and used indirect immunofluorescence (IIF) to detect antiperinuclear factor antibodies in RA sera. Most scholars now believe that the antigen of APF exists in the keratin hyaline protein granules of human buccal mucosa cells, and its component may be the medium fibrillar binding protein of epithelial cells or its precursor, namely (pro)Filaggrin, APF has high sensitivity and specificity for RA diagnosis. The sensitivity and specificity reported by Anhui Provincial Hospital were 65.9% and 97.5%, respectively; 28.6% and 95% reported by Cordonnier and 42.1% and 90% reported by Gaby. It can be seen that APF has high specificity for the early diagnosis of RA, and APF antibodies can appear early in the course of RA, independent of the patient’s age and disease duration, and do not correlate with RF; some scholars have found a correlation between APF and polyarticular involvement, morning stiffness and bone destruction. In recent years, more advocate 1:80 (100) as the positive threshold, that can improve the specificity, and sensitivity loss is not much. Anti-Sa antibodies were first reported by Menard in 1989, Sa antigen was extracted from human spleen or placenta, and the detection of Sa antibodies can be done by immunoblotting and IIF method. The presence of high concentrations of Sa antigen in RA synovial tissue suggests that anti-Sa antibodies are a potentially important pathological player in the pathogenesis of RA. The sensitivity and specificity of anti-Sa antibodies were 39.8% and 92.1% in Gilles and 33.6% and 90.6% in Peking Union Medical College. If IgG anti-Sa antibodies are measured by immunospotting in the first year of RA onset, serious bone destruction will occur. In 1998, Gerard et al. in the Netherlands used ELISA to detect a specific autoantibody called anti-cyclic citrullinated polypeptide (anti-CCP) in the sera of RA patients, and found that it has high sensitivity and specificity for RA, and in patients with early rheumatoid arthritis, the specificity of this antibody was 96%. The specificity of this antibody was 96% in patients with early rheumatoid arthritis, and the specificity of its counterpart, IgM-RF (ELISA), was 91%, with a positive predictive value of 84% for the anti-CCP antibody by follow-up. The results also showed that the specificity could be increased to 98% if RF was combined with anti-CCP. At the subsequent one-year follow-up, the sensitivity of anti-CCP was found to decrease from 54% to 49%, while RF increased from 48% to 53%, suggesting that anti-CCP antibodies are of greater diagnostic value in the early stages of RA.