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Background: The acute sickness response to infection is a stereotyped set of illness manifestations initiated by proinflammatory signals in the periphery but mediated centrally. P2RX7 is a highly polymorphic gene encoding an ATP-gated cationic pore, widely expressed on immune cells and the brain, and regulating the NLRP3 inflammasome, as well as diverse neural functions., Methods: Associations between P2RX7 genotype, pore activity, and illness manifestations were examined in a cohort with acute viral and bacterial infections (n = 484). Genotyping of 12 P2RX7 function-modifying single-nucleotide polymorphisms (SNPs) was used to identify haplotypes and diplotypes. Leucocyte pore activity was measured by uptake of the fluorescent dye, YO-PRO-1, and by ATP-induced interleukin-1β (IL-1β) release. Associations were sought with scores describing the symptom domains, or endophenotypes, derived from principal components analysis., Results: Among the 12 SNPs, a 4-SNP haplotype block with 5 variants was found in 99.5% of the subjects. These haplotypes and diplotypes were closely associated with variations in pore activity and IL-1β production. Homozygous diplotypes were associated with overall illness severity as well as fatigue, pain, and mood disturbances., Conclusions: P2RX7 signaling plays a significant role in the acute sickness response to infection, likely acting in both the immune system and the brain., (© The Author(s) 2021. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.)

Background and Objectives: In the absence of effective pharmacotherapy, there is an urgent need to test evidence-based dementia care interventions using pragmatic trial approaches. We present results from a study in which an evidence-based, nonpharmacologic intervention for persons living with Alzheimer's disease and related dementia (ADRD) and their informal caregivers, Care of Persons with Dementia in their Environments (COPE), was tested in a Medicaid and state revenue-funded home and community-based service (HCBS) program., Research Design and Methods: Using pragmatic trial design strategies, persons living with ADRD and their caregivers were randomly assigned as dyads to receive COPE plus usual HCBS (COPE; n = 145 dyads) or usual HCBS only (Usual Care or UC; n = 146 dyads). Outcomes were measured prerandomization, and 4 and 12 months postrandomization. Outcomes for persons living with ADRD included functional independence, activity engagement, self-reported quality of life, and behavioral and psychological symptoms. Caregiver outcomes included perceived well-being, confidence using dementia management strategies, and degree of distress caused by behavioral and psychological symptoms., Results: After 4 months, caregivers receiving COPE reported greater perceived well-being (least squares mean = 3.2; 95% CI: 3.1-3.3) than caregivers receiving UC (3.0; 2.9-3.0; p < .001), and persons living with ADRD receiving COPE, compared to those receiving UC, showed a strong trend toward experiencing less frequent and less severe behavioral and psychological symptoms (9.7; 5.2-14.2 vs 12.7; 8.3-17.1; p = .07). After 12 months, persons living with ADRD receiving COPE were more engaged in meaningful activities (2.1; 2.0-2.1 vs 1.9; 1.9-2.0; p = .02) than those receiving UC., Discussion and Implications: Embedding COPE in a publicly funded HCBS program yielded positive immediate effects on caregivers' well-being, marginal positive immediate effects on behavioral and psychological symptoms, and long-term effects on meaningful activity engagement among persons living with ADRD. Findings suggest that COPE can be effectively integrated into this service system, an important step towards widespread adoption., Clinical Trials Registration Number: NCT02365051., (© The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America.)

Background: Inflammatory bowel disease (IBD) entails a higher risk of infections, including those that could be prevented with immunizations. Current Advisory Committee on Immunization Practices and American College of Gastroenterology vaccine recommendations for patients with IBD are based on low levels of evidence., Methods: We conducted a population-based descriptive cohort study using the US National Inpatient Sample ICD-9 codes from 2012 to 2015. We measured the frequency of patients with IBD who were admitted to the hospital with a vaccine-preventable disease (VPD). Frequencies and demographics were determined and compared between patients with IBD and patients without IBD., Results: Of discharges, 596,485 (2.08%) were secondary to a VPD, and 7180 (1.2%) were found to have both a VPD and IBD (including Crohn disease and ulcerative colitis). The most common VPDs among patients with IBD were herpes zoster virus (HZV) (34.9%) and hepatitis B virus (31.6%), followed by influenza (22.1%). Pneumococcal pneumonia (9.1%) and hepatitis A virus (2.4%) were less common. Inpatients with IBD were twice as likely to have HZV when compared to non-IBD inpatients (odds ratios [OR] = 2.30 [95% CI, 2.06-2.58], P < 0.0001) This finding was consistent for every study year. Pneumococcal pneumonia [OR = 0.62 (95% CI, 0.52-0.74), P < 0.0001] and influenza [OR = 0.72 (95% CI, 0.63-0.81), P < 0.0001] were significantly lower in the IBD population. There was no difference for other VPDs., Conclusions: HZV was the most frequent VPD in IBD inpatients. Patients with IBD have a higher rate of hospital admissions with HZV and a lower rate of pneumococcal pneumonia and influenza admissions when compared with non-IBD patients. For other VPDs, patients with IBD have the same rate of admission as the general population., (© 2019 Crohn’s & Colitis Foundation. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Stem cell (SC) division, deployment, and differentiation are processes that contribute to corneal epithelial renewal. Until now studying the destiny of these cells in a living mammal has not been possible. However, the advent of inducible multicolor genetic tagging and powerful imaging technologies has rendered this achievable in the translucent and readily accessible murine cornea. K14CreER(T2)-Confetti mice that harbor two copies of the Brainbow 2.1 cassette, yielding up to 10 colors from the stochastic recombination of fluorescent proteins, were used to monitor K-14(+) progenitor cell dynamics within the corneal epithelium in live animals. Multicolored columns of cells emerged from the basal limbal epithelium as they expanded and migrated linearly at a rate of 10.8 µm/day toward the central cornea. Moreover, the permanent expression of fluorophores, passed on from progenitor to progeny, assisted in discriminating individual clones as spectrally distinct streaks containing more than 1,000 cells within the illuminated area. The centripetal clonal expansion is suggestive that a single progenitor cell is responsible for maintaining a narrow corridor of corneal epithelial cells. Our data are in agreement with the limbus as the repository for SC as opposed to SC being distributed throughout the central cornea. This is the first report describing stem/progenitor cell fate determination in the murine cornea using multicolor genetic tracing. This model represents a powerful new resource to monitor SC kinetics and fate choice under homeostatic conditions, and may assist in assessing clonal evolution during corneal development, aging, wound-healing, disease, and following transplantation., (© 2014 AlphaMed Press.)

The adult cornea harbors stem cells (SCs) in its periphery, in a niche known as the limbus. Over the past 2 decades there has been substantial research into these adult corneal SCs, their limbal niche, and their therapeutic applications. However, few studies have investigated how this niche and its SCs develop in humans. To better characterize this development, human fetal corneas from 8.5- to 22-weeks'-gestation (n = 173), neonatal (n = 2), and adult (n = 10) specimens were obtained. Histological and immunohistochemical assessments were conducted to determine embryological changes and expression of developmental and SC-related genes. Fresh fetal corneas were explanted to propagate corneal progenitors and cells characterized using reverse transcription-polymerase chain reaction, immunohistochemistry, flow cytometry, and colony-forming assays. A novel "ridge-like" structure was identified, circumscribing the fetal cornea, which we hypothesize represents the rudimentary SC niche. Immunohistochemistry disclosed "stem-like" cells across the cornea, becoming confined to this ridge with increasing gestational age. In addition, for the first time, pure long-term cultures of fetal corneal epithelium, which displayed phenotypical and functional properties similar to those of adult limbal SCs, were established. Optimization of culture techniques and purification of this SC population will allow for further investigation of their proliferative ability, with potential research and clinical applications. This study expands our understanding of limbal niche development and opens new avenues for investigation.

Background: The use of verbal orders has been identified as a potential contributor to poor quality and less safe care. As a result, many organisations have encouraged changing the verbal orders process and/or reducing/eliminating verbal orders altogether (Joint Commission (2005), Institute of Medicine (2001), Leapfrog organisation, Institute of Safe Medication Practices). Ironically there is a paucity of research evidence to support the widespread concern over verbal order., Aims: This paper describes the very limited existing research on verbal orders, presents a model of verbal order use identifying potential error trigger points and suggests a verbal order research agenda in order to better understand the nature and extent of the potential patient care safety threat posed by verbal orders.

Background: Functional polymorphisms in immune response genes are increasingly recognized as important contributors to the marked individual differences in susceptibility to and outcomes of infectious disease. The acute sickness response is a stereotypical set of illness manifestations mediated by the proinflammatory cytokines induced by many different pathogens. The genetic determinants of severity of the acute sickness response have not previously been explored., Methods: We examined the impact of functional polymorphisms in cytokine genes with critical roles in the early immune response (tumor necrosis factor-alpha, interleukin-6, interleukin-10, and interferon-gamma) on the severity and duration of illness following acute infection with Epstein-Barr virus, Coxiella burnetii (the causative agent of Q fever), or Ross River virus., Results: We found that the interferon-gamma +874T/A and the interleukin-10 -592C/A polymorphisms significantly affected illness severity, cytokine protein levels, and the duration of illness. These cytokine genotypes acted in synergy to potentiate their influence on disease outcomes., Conclusions: These findings suggest that genetically determined variations in the intensity of the inflammatory response underpin the severity of the acute sickness response and predict the recovery time across varied infections.

Peripheral blood specimens and clinical data were obtained over a 12-month period from subjects in the Dubbo Infection Outcomes Study to examine cytokine production in postinfective fatigue syndrome. Ex vivo production of 8 cytokines was examined in 22 case patients and in 42 control subjects who recovered promptly. No significant differences were found. Ongoing production of the cytokines examined does not play a role in postinfective fatigue syndrome.

Background: Infectious mononucleosis (IM) commonly triggers a protracted postinfective fatigue syndrome (PIFS) of unknown pathogenesis., Methods: Seven subjects with PIFS with 6 or more months of disabling symptoms and 8 matched control subjects who had recovered promptly from documented IM were studied. The expression of 30,000 genes was examined in the peripheral blood by microarray analysis in 65 longitudinally collected samples. Gene expression patterns associated with PIFS were sought by correlation with symptom factor scores., Results: Differential expression of 733 genes was identified when samples collected early during the illness and at the late (recovered) time point were compared. Of these genes, 234 were found to be significantly correlated with the reported severity of the fatigue symptom factor, and 180 were found to be correlated with the musculoskeletal pain symptom factor. Validation by analysis of the longitudinal expression pattern revealed 35 genes for which changes in expression were consistent with the illness course. These genes included several that are involved in signal transduction pathways, metal ion binding, and ion channel activity., Conclusions: Gene expression correlates of the cardinal symptoms of PIFS after IM have been identified. Further studies of these gene products may help to elucidate the pathogenesis of PIFS.

Background: Primary Epstein-Barr virus (EBV) infection causes a spectrum of characteristics that range from asymptomatic seroconversion to severe infectious mononucleosis (IM), sometimes with prolonged symptoms and disability. We examined the relationships between clinical course, number of viral copies, and immunological parameters in a prospective cohort of subjects with recent IM., Methods: Eight case patients with at least 6 months of disabling symptoms and 31 matched control subjects who had recovered promptly were included. Symptom scores were recorded at regular intervals over the course of 12 months. Cellular EBV load, EBV-specific antibody responses, lymphocyte subsets, and EBV-specific interferon (IFN)- gamma induction were measured., Results: In case patients with prolonged illness, the severity of acute-phase symptoms was greater, the development of anti-EBV nuclear antigen-1 immunoglobulin G was more rapid, and the time to development of the peak IFN- gamma response to the majority of latent-cycle EBV peptides was generally slower than those in control subjects. However, in both groups, neither viral nor immune parameters correlated with the severity or duration of symptoms., Conclusions: The resolution of symptomatic IM is not determined by control of viremia, nor is it easily explained by altered host responses to EBV infection. The detailed determinants of delayed recovery remain to be elucidated.

The diagnosis of pulmonary tuberculosis (TB) in a nursery teacher led to a total of 282 adults and children being screened for TB, and 67 of these contracted the condition. Latent and active factors mitigated against earlier diagnosis of the disease during the multiple contacts by the teacher with the healthcare system over 18 months. A series of barely inter-linked events meant that the system failed the patient and consequently the contacts who contracted the disease. The system errors were widespread and render possible a similar occurrence elsewhere.

Lymph nodes are the major site of cell-to-cell transmission and replication of HIV-1. Trafficking of CD4+ T lymphocytes into lymph nodes provides a continual supply of susceptible target lymphocytes, and conversely, recruitment of CD8+ T lymphocytes may be critical for the host response that attempts to control HIV-1 replication. The present study was undertaken as no detailed assessment of lymphocyte subpopulations in HIV-1-infected lymph nodes has previously been reported. Peripheral blood and single-cell suspensions prepared from lymph nodes of patients with HIV-1 and control subjects were analysed using three-colour flow cytometry. Approximately 80% of the lymphocytes in control lymph nodes were CD3+ T lymphocytes, of which over 65% were CD4+. The majority of the CD4+ and CD8+ T lymphocytes obtained from both lymph nodes and blood of control subjects were immunologically naive (CD45RA+). By contrast, in HIV-1-infected patients there was a significant reduction in the proportion of CD4+ T lymphocytes and an expansion of the CD8+ T lymphocyte subset in both lymph nodes and peripheral blood. Furthermore, a high proportion of these T lymphocytes displayed a marker for immunological memory (CD45RO+). T lymphocytes derived from HIV-1-infected lymph nodes also showed altered expression of the adhesion molecules, L-selectin and very late antigen-4 (VLA-4), but not leucocyte function-associated antigen-1 (LFA-1). In an in vitro adhesion assay, lymphocytes from HIV-1-infected nodes were significantly more adhesive than control lymphocytes on fibronectin, as well as recombinant human intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) substrates. This combination of altered lymphocyte subpopulations in the HIV-1-infected lymph nodes, as well as enhanced adhesion phenotype and function, suggests that T lymphocyte traffic to lymph nodes in HIV disease may be an important determinant of pathogenesis.

Objective: To investigate the expression and source of chemokines in minor salivary gland biopsies (MSGs) in patients with Sjögren's syndrome (SS)., Methods: Immunohistochemical analysis was used to determine the pattern of chemokine expression in MSGs from patients with (n=6) and without (n=5) SS, as well as to examine the phenotype of both resident and infiltrating cells expressing chemokines., Results: Significant differences in the number of infiltrating mononuclear (MN) cells in patients with and without SS were noted. Ductal epithelial cells of SS biopsies expressed significantly increased levels of macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, interleukin-8 (IL-8) and RANTES (Regulated upon Activation, Normal T cell Expressed and Secreted). Biopsies from patients with SS showed that MIP-1beta was expressed by 51% of infiltrating cells, while 41% expressed MIP-1alpha, whereas 22 and 7% expressed RANTES and IL-8, respectively., Conclusion: Chemokines expressed by ductal epithelial cells may attract circulating leucocytes, in particular CD4+ T cells, towards the site of inflammation, thereby orchestrating the influx of MN cells characteristically seen in MSGs in SS. Chemokines may be induced directly by a putative triggering agent for SS, or secondary to the release of pro-inflammatory cytokines produced by epithelial cells. These findings further implicate epithelial cells as playing a major role in the pathogenesis of SS and implicate chemokines in the leucocyte recruitment in this setting.

Tumor necrosis factor-alpha (TNF-alpha) is a potent pro-inflammatory cytokine and mediator of the inflammatory response. It has been implicated in the pathogenesis of many inflammatory disorders, including rheumatoid arthritis (RA), septic shock, and Crohn's disease. Using a specific anti-human TNF-alpha antibody we detected immunoreactivity for this cytokine in the cytoplasm of inflammatory cells in several chronic inflammatory disorders, including RA, scleritis, and polyarteritis nodosa. These cells were identified predominantly as IgG-expressing plasma cells. Lymph nodes from patients with Hodgkin's lymphoma and breast cancer, but not from control subjects, were also found to contain TNF-alpha-positive plasma cells. Cultured EBV-B lymphocytes and a human plasma cell line (ARH-77) when stimulated with phorbol myristate acetate demonstrated cytoplasmic TNF-alpha immunoreactivity. Western blot analysis of cell membranes and conditioned media from both cell types revealed the presence of the 26-kDa membrane-bound from and the 17-kDa soluble from of TNF-alpha, respectively. TNF-alpha was quantitated by enzyme-linked immunosorbent assay and found to be biologically active as determined by the L929 cytotoxicity assay. This is the first demonstration that plasma cells may be capable of modulating immune and inflammatory responses, not only by antibody production, but also by their secretion of a key inflammatory mediator, TNF-alpha.

We have studied the relationship between the cytokine production induced in vivo by prolonged isometric exercise and the symptom complex marked by fatigue in patients with chronic fatigue syndrome (CFS). Twelve male patients and 13 matched male control subjects undertook an isometric hand-grip exercise protocol utilizing dynamometers. Subjects undertook 30 minutes of exercise, for which the target force was set at 40% of the maximal voluntary contraction and the duty cycle was 50%. Prior to, during, and for 24 hours following the exercise, blood samples were collected and assayed for the presence of cytokines, including interferon-gamma and interferon-alpha, interleukin-1 beta, and tumor necrosis factor-alpha. At those times subjects also completed the Profile of Mood States (POMS) questionnaire, which served as a measure of changes in subjective fatigue. No significant alteration in the level of any of the cytokines in the plasma of patients or control subjects was detected before, during, or after exercise. Surprisingly, the patients' levels of fatigue, depression, and confusion, as measured by the POMS, decreased in response to the exercise. These data do not confirm the presence of an immunologic process correlating with the exacerbation of fatigue after exercise experienced by patients with CFS. Limitations in the study design and in the sensitivity of the cytokine assays may have affected our results.

The chronic fatigue syndrome (CFS) is characterized by severe persistent fatigue and neuropsychiatric symptoms. It has been proposed that the abnormalities in cell-mediated immunity which have been documented in patients with CFS may be attributable to a clinical depression, prevalent in patients with this disorder. Cell-mediated immune status was evaluated in patients with carefully defined CFS and compared with that of matched subjects with major depression (non-melancholic, non-psychotic) as well as healthy control subjects. Patients with CFS demonstrated impaired lymphocyte responses to phytohaemagglutinin (PHA) stimulation, and reduced or absent delayed-type hypersensitivity (DTH) skin responses when compared either with subjects with major depression or with healthy control subjects (P less than 0.05 for each analysis). Although depression is common in patients with CFS, the disturbances of cell-mediated immunity in this disorder differ in prevalence and magnitude from those associated with major depression. These observations strengthen the likelihood of a direct relationship between abnormal cell-mediated immunity and the etiology of CFS.

We examined the expression of HLA antigens on post-mortem human uveal tissues and on cultured uveal cells. There was no in vivo expression of class I or class II antigens in these tissues, except for the blood vessel endothelium which expressed class I but not class II antigens. Tissue cultured uveal cells were found to express class I antigens. The effect of interferon-alpha and interferon-gamma on the in vitro expression of these antigens was examined. Class I HLA antigen expression was enhanced by both interferon-alpha and interferon-gamma, while class II HLA antigens were induced on up to 100% of cultured cells, but only by interferon-gamma. These findings are discussed in their relation to immune mechanisms occurring in ocular inflammatory disorders.

The relationship between HLA B27 anterior uveitis (AU) and evidence of chlamydia trachomatis infection was investigated in 35 consecutive patients attending a uveitis research clinic, using a complement fixation test and lymphocyte transformation test to chlamydia (ornithosis-psittacosis) group antigen. A significant stimulation index (SI greater than 2) was found in 73% (11/15) of the HLA B27 positive patients compared with the HLA B27 negative AU patients and controls (P less than 0.03). There was no difference between AU patients with and without associated rheumatic disease or in terms of antibody response. The results of the present study indicate a significant relationship between the cell-mediated immune response to chlamydia group antigen and the HLA B27 positive subgroup of patients with AU.

We have previously reported the association of Chlamydia trachomatis with HLA B27+ related diseases. To investigate the possibility that chlamydial antibodies serve to localize the immune response in such diseases, we examined the crossreactivity of chlamydial antibodies (rabbit anti-D and anti-L2 serotypes) with peripheral blood mononuclear cells of patients with ankylosing spondylitis (AS) and anterior uveitis (AU) and with human and bovine ocular tissue and cells in culture. Our results indicate a significantly increased percentage binding of chlamydial antibody (D serotype) to the mononuclear cells of HLA B27+ patients with AS when compared with HLA B27- patients with AS (12.9% +/- 2.2 versus 5.4% +/- 2.2), B27+ controls (5.5% +/- 1.5) and B27- controls (6.1% +/- 1.0). There was no significant difference between controls and HLA B27+ patients with AU (6.6% +/- 1.9) and B27- patients with AU (8.7% +/- 1.1). This crossreactivity could not be blocked by monoclonal HLA B27 antibody. Chlamydial antibodies (D and L2) crossreact with human and bovine conjunctiva but not uvea, tissue culture derived iris fibroblasts or smooth muscle cells. Our results provide additional support for the concept of crossreactivity between antibodies to microbial agents and peripheral blood mononuclear cells of patients with HLA B27+ AS.

The purpose of this study was to examine the efficacy of the oxacillin disk diffusion test and the methicillin and oxacillin agar screen tests as predictors of oxacillin resistance as defined by the reference broth microdilution method. A total of 444 clinical isolates of Staphylococcus aureus collected from individual patients over a four-year period were tested by (1) the oxacillin disk diffusion test, with particular attention to the presence of fine growth of a resistant subpopulation within the zone of inhibition (Ox Grow interpretive criteria); (2) the agar screen method using agar plates with 4% NaCl and either 6 mg/L oxacillin or 10 mg/L methicillin; and (3) the oxacillin and methicillin broth microdilution test methods with 2% NaCl supplementation. Overall, 62 (14%) isolates were resistant and 382 (86%) isolates were susceptible to oxacillin with the use of the reference broth microdilution system. The results indicate that the disk diffusion test with the use of the Ox Grow criteria had a high sensitivity (94%) and negative predictive value (98%) but a low specificity (67%) and positive predictive value (32%) when compared with the reference broth dilution test. Similarly, the agar screen tests had a high sensitivity (95-97%) and negative predictive values (99%) but low specificity (64-74%) and positive predictive values (30-37%). These data indicate that the agar screen tests and the oxacillin disk test with the use of the Ox Grow interpretive criteria may be useful as screening tests for detecting resistance to the penicillinase-resistant penicillins but that all resistant isolates should be confirmed by the reference broth dilution method because of the large number of false-resistant screening test results.

Refinements in testing for resistance to penicillinase-resistant penicillins (PRP) in Staphylococcus aureus have resulted in confusion in classifying isolates as PRP susceptible or resistant. Specifically, a group of organisms has been identified that produce large amounts of beta-lactamase and appear borderline resistant. These organisms have been called "occult resistant" or "acquired oxacillin-resistant" S. aureus (AORSA). A retrospective study was conducted to evaluate the implication of this in vitro phenomenon in managing patients with AORSA infections. Among 134 patients with S. aureus infections, 89 were infected with oxacillin-susceptible S. aureus (OSSA), 26 with AORSA, and 19 with oxacillin-resistant S. aureus (ORSA). There were no significant differences in outcomes when OSSA and AORSA infections were treated with PRP (chi 2MH = .990; P = .32). These results do not suppor the contention that AORSA infections should be managed differently from OSSA infections. Identifying AORSA may not be helpful in guiding antimicrobial therapy or predicting the outcome of infections with AORSA.

In an effort to assess the degree of methodologic variation and adherence to current guidelines for detection of methicillin-resistant Staphylococcus aureus (MRSA), the authors surveyed the susceptibility testing practices of all 162 microbiology laboratories in the Veterans Administration (VA) system. Completed questionnaires were returned by 136 (84%) of the laboratories. Overall, 96 (71%) laboratories used disk diffusion testing, 54 (40%) used manual broth dilution, and 36 (26%) used an automated method. The percentage of MRSA detected ranged from 0 to 52%, with a mean of 10%. In general, fewer than 60% of laboratories followed the current susceptibility testing guidelines for key methodologic variables such as inoculum preparation, duration of incubation, and medium supplementation. Failure to adhere to these guidelines may result in suboptimal detection of MRSA.

The chemiluminescent (CL) associated phagocytic response of peripheral blood monocytes to two serovars of Chlamydia trachomatis, Shigella flexneri and zymosan was assessed in a group of 26 patients with anterior uveitis (AU). HLA-B27+ patients with AU, when compared to HLA-B27- patients with AU and appropriate controls, had a significantly decreased CL response to C. trachomatis but no difference between groups in the response to S. flexneri and zymosan. The decreased chemiluminescent (phagocytic) response of mononuclear phagocytes to Chlamydiae may indicate an important abnormality in the pathogenesis of HLA-B27+ AU.