Disease relevance of Lymphocytosis

• One patient with progressing lymphocytosis, anemia, and thrombocytopenia despite 10 courses of fludarabine entered a complete remission when treated with 2-chlorodeoxyadenosine [1].
• CD8 lymphocytosis and pseudotumoral splenomegaly in HIV infection [2].
• One patient treated with pulse steroid therapy had reversal of lymphocytosis and severe neutropenia with subsequent resolution of an intractable infection [3].
• IL-2 infusions produced an initial lymphopenia, followed by a progressive recovery in mononuclear cell numbers and a rebound lymphocytosis after the termination of treatment [4].
• While Fas-deficient mice display marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51-/- mice had no apparent defects in secondary lymphoid organs [5].

High impact information on Lymphocytosis

• To test this hypothesis, 22 Ghanaian patients with HMS and/or lymphocytosis were categorised by degree of response to proguanil according to standard clinical criteria, and DNA was extracted from peripheral blood cells and screened for rearrangements of the Jh region of the immunoglobulin gene with a DNA probe [6].
• In addition, the Fas-null mice showed lymphocytosis, accompanied by lymphocytic infiltration in the lungs and liver [7].
• Before treatment, exhaustive exercise according to the Bruce protocol led to a marked lymphocytosis [8].
• In healthy subjects, exercise increased plasma norepinephrine and epinephrine and caused lymphocytosis [9].
• IL-2 induced lymphocytosis, with an increase in CD56+ and CD8+ cells [10].

Chemical compound and disease context of Lymphocytosis

• Lymphocytes from patients with acute and chronic T-cell malignancy or chronic T gamma lymphocytosis were characterized by studying the activity of three enzymes involved in purine metabolism and by determining the isoenzyme pattern of lactate dehydrogenase (LDH) in addition to analysis of surface marker expression with monoclonal antibodies [11].
• This increase correlated with an increase in the number of circulating B lymphocytes as demonstrated by the presence of surface immunoglobulins (SIg) and a high cell proliferative response to lipopolysaccharide and was considered to be a persistent B cell lymphocytosis [12].
• Disease activity was based on serum angiotensin converting enzyme activity and/or lymphocytosis at bronchoalveolar lavage [13].
• A 64-year-old man developed a severe generalized pruritic morbilliform skin eruption, fever, eosinophilia, atypical lymphocytosis, and liver dysfunction 30 days after ingestion of mexiletine, a sodium channel blocker, prescribed to treat postherpetic neuralgia [14].
• Plasma cyclosporine levels did not correlate with IV or graft lymphocytosis [15].

Biological context of Lymphocytosis

• Although IL-2 is commonly thought to promote proliferation of T lymphocytes, mice deficient in IL-2 exhibit splenomegaly, lymphocytosis, and autoimmunity, suggesting this cytokine may have a prominent role in T cell homeostasis [16].
• In contrast to the common form of polyclonal lymphocytosis, this case was not associated with HLA-DR7 and/or abnormalities of chromosome 3, p53 or Bcl2/IgH [17].
• Healthy subjects developed airway inflammation 6 h after DE exposure, with airways neutrophilia and lymphocytosis together with an increase in interleukin-8 (IL-8) protein in lavage fluid, increased IL-8 messenger ribonucleic acid expression in the bronchial mucosa and upregulation of the endothelial adhesion molecules [18].
• A diagnosis of SLVL was made, based on tartrate-resistant acid phosphatase-negative peripheral villous lymphocytosis with CD19+, CD20+, HLA-DR+ phenotypes, and the involvement of spleen white pulp with these cells [19].
• All subunits were inactive in histamine sensitization, lymphocytosis, and hemagglutination assays [20].

Anatomical context of Lymphocytosis

• The expression of EB6 and GL183 surface antigens has been analyzed in a series of 14 patients with lymphoproliferative disease of granular lymphocytes (LDGL) characterized by a chronic CD3-CD16+ lymphocytosis [21].
• This syndrome, which is strongly associated with rheumatoid arthritis, is characterized by peripheral blood and bone marrow lymphocytosis and neutropenia, red cell aplasia, or both [22].
• Twenty-seven patients with familial encephalopathy with calcification of the basal ganglia and chronic cerebrospinal fluid (CSF) lymphocytosis (Aicardi-Goutières syndrome) are reviewed [23].
• The results show that IL-2 is more biologically active by CIV than q8h administration, as demonstrated by greater rebound lymphocytosis, LAK cell yield, and in vivo immunostimulation [24].
• Aicardi-Goutières syndrome (Mendelian inheritance in man Catalog No *225750) is an autosomal recessive encephalopathy which causes developmental arrest, intracerebral calcification, and white matter disease in the presence of chronic cerebrospinal fluid lymphocytosis, and a raised level of cerebrospinal fluid interferon-alpha (IFN-alpha) [25].

Gene context of Lymphocytosis

• However, the ADA activity and/or the ADA/PNP ratio were consistently higher in the cells from the patients with chronic T gamma lymphocytosis than in those with chronic T malignancy [11].
• Polymorphism in BoLA-DRB3 exon 2 correlates with resistance to persistent lymphocytosis caused by bovine leukemia virus [26].
• Additionally, during persistent lymphocytosis, peak IL-2 and IL-10 mRNA expression was delayed, and elevated expression was prolonged [27].
• All cases showed monoclonal CD5/CD19-positive lymphocytosis, with more than 10% large lymphocytes and/or prolymphocytes in peripheral blood smears and reactivity with FMC7, or bright expression of surface immunoglobulins in a fraction of the cases [28].
• Although CCND1 expressing SLVL more commonly had marked lymphocytosis, they did not demonstrate a more aggressive clinical course than their negative counterparts, demonstrating that the detection of CCND1 expression or of a t(11;14) should not suffice to alter diagnostic classification in the absence of other criteria [29].

Analytical, diagnostic and therapeutic context of Lymphocytosis

• Mild colonic lymphocytosis in patients with untreated celiac sprue should be distinguished from lymphocytic colitis by the lack of surface epithelial abnormalities, the lack of increased cellularity of the lamina propria, and the lack of ongoing watery diarrhea after treatment with a gluten-free diet [30].
• The immunophenotype of blood lymphocytosis using flow cytometry, the presence of a t(11;14)(q13;q32) and a cyclin D1 expression by leukaemic cells all fit with the diagnosis of MCL [31].
• Development of antibody titres in non-vaccinated children with whooping cough of different duration (all confirmed by positive culture) were investigated by ELISA using lymphocytosis promoting factor (LPF, pertussis toxin), filamentous haemagglutinin (FHA), 69 kDa protein and lipopolysaccharide (LPS) as antigens [32].
• Both thymoma and lymphocytosis were improved by a combination of chemotherapy and mediastinal irradiation [33].
• In this case a tissue-based polymerase chain reaction (PCR) analysis of T-cell receptor (TCR) beta and gamma gene rearrangements proofed to be essential in confidently distinguishing multifocal monoclonal intramucosal T-cell lymphocytosis from an intense reactive inflammatory infiltrate in celiac disease (CD) [34].

References