Context: As teaching hospitals institute social distancing and defer non-emergent procedures to cope with the coronavirus disease 2019 (COVID-19) pandemic, the need for daily onsite presence, unless necessary has been reduced for all medical staff including trainees. Pathology training programs must adapt to these changes to ensure overall safety without significantly compromising training and educational mission of the institution. Objective: To describe the hybrid on-site and remote anatomic pathology training model in response to the COVID-19 pandemic, which was implemented in our pathology department and report the clinical fellows' responses to the survey about their experiences. Design: The hybrid model was implemented March 25, 2020. Fellows alternate weekly between working on-site and working remotely. On-site, fellows wear personal protective equipment and maintain social distancing. Remotely, fellows use digital pathology to review cases and supplement with online educational activities. Virtual “coffee breaks,” meditation, and exercise are part of the curriculum. Online platforms, including WebEx, Google Classroom, and Canvas, are used to continue educational activities. The survey was open May 19 through June 8. Results: Twenty-eight of the 29 clinical fellows (96%) responded. Many of the respondents indicated substantial increase in their skill with using digital pathology and online platforms during the pandemic. The top most helpful resources were the United States and Canadian Academy of Pathology Interactive Microscopy courses (22/23=91% of clinical fellows found very or somewhat helpful), ExpertPath (19/23=82%), the College of American Pathologists virtual learning series (18/23=78%), the World Health Organization Blue Books (16/23=70%), the American Society of Cytopathology webinars (14/23=61%), and our institutional digital slide collection (12/23=52%). Conclusions: Hybrid on-site and remote training can maximize anatomic pathology learning opportunities while maintaining the safety of trainees, hospital personnel, and the community.

Graft-versus-host disease (GvHD) is a common, morbid complication after intestinal transplantation (ITx) with poorly understood pathophysiology. Resident memory T cells (T RM ) are a recently described CD69+ memory T cell subset localizing to peripheral tissue. We observed that T effector memory cells (T EM ) in the blood increase during GvHD and hypothesized that they derive from donor graft CD69+T RM migrating into host blood and tissue. To probe this hypothesis, graft and blood lymphocytes from 10 ITx patients with overt GvHD and 34 without were longitudinally analyzed using flow cytometry. As hypothesized, CD4+ and CD8+CD69+T RM were significantly increased in blood and grafts of GvHD patients, alongside higher cytokine and activation marker expression. The majority of CD69+T RM were donor derived as determined by multiplex immunostaining. Notably, CD8/PD-1 was significantly elevated in blood prior to transplantation in patients who later had GvHD, and percentages of HLA-DR, CD57, PD-1, and naïve T cells differed significantly between GvHD patients who died vs. those who survived. Overall, we demonstrate that (1) there were significant increases in T EM at the time of GvHD, possibly of donor derivation; (2) donor T RM in the graft are a possible source; and (3) potential biomarkers for the development and prognosis of GvHD exist.

DEL red blood cells (RBCs) type as D– by routine serologic methods and are transfused routinely, without being identified as expressing a very weak D antigen, to D– recipients. DEL RBCs are detected only by adsorption and elution of anti-D or by molecular methods. Most DEL phenotypes have been reported in population studies conducted in East Asia, although DEL phenotypes have been detected also among Caucasian individuals. Approximately 98 percent of DEL phenotypes in East Asians are associated with the RHD*DEL1 or RHD*01EL.01 allele. The prevalence of DEL phenotypes has been reported among D– Han Chinese (30%), Japanese (28%), and Korean (17%) populations. The prevalence of DEL phenotypes is significantly lower among D– Caucasian populations (0.1%). Among the 3–5 percent of African individuals who are D–, there are no reports of the DEL phenotype. Case reports from East Asia indicate that transfusion of DEL RBCs to D– recipients has been associated with D alloimmunization. East Asian immigrants constitute 2.1 percent of the 318.9 million persons residing in the United States, and an estimated 2.8 percent are blood donors. Using these statistics, we estimate that 68–683 units of DEL RBCs from donors of East Asian ancestry are transfused as D– annually in the United States. Given the reports from East Asia of D alloimmunization attributed to transfusion of DEL RBCs, one would expect an occasional report of D alloimmunization in the United States following transfusion of DEL RBCs to a D– recipient. If such cases do occur, the most likely reason that they are not detected is the absence of active post-transfusion monitoring for formation of anti-D. Immunohematology 2017;33:125–132.

Positive staining for PD-L1 may be a prognostic marker for decreased survival in esophageal adenocarcinoma. Additional TIL cell types should be investigated for creation of an esophageal cancer Immunoscore. PD-L1 has potential as a therapeutic target.

Diffuse large B-cell lymphoma (DLBCL) is characterized by medium- to large-sized neoplastic cells that express a wide range of B-cell markers including CD19, CD20, CD22, and CD79a. Also, as this is a hematopoietic malignancy, there is expression of the leukocyte common antigen CD45. Lack of CD20 expression occurs in a specific rare heterogeneous subgroup of DLBCL including primary effusion lymphoma, plasmablastic lymphoma, ALK-positive large B-cell lymphoma, and large B-cell lymphoma arising in HHV8+ multicentric Castleman disease. In this article, we report a rare case of CD20- and CD45-negative Epstein-Barr virus-positive DLBCL in which the entities listed above were ruled out, thereby posing a significant diagnostic challenge. Arriving at the correct diagnosis of Epstein-Barr virus-positive DLBCL was supported by immunoreactivity for the B-cell transcription factor Oct-2 and the pan-B cell marker CD79a.