Non-prescriptional use of medicinal herbs among cancer patients is common around the world. The alleged anti-cancer effects of most herbal extracts are mainly based on studies derived from in vitro or in vivo animal experiments. The current information suggests that these herbal extracts exert their biological effect either through cytotoxic or immunomodulatory mechanisms. One of the active compounds responsible for the immune effects of herbal products is in the form of complex polysaccharides known as β-glucans. β-glucans are ubiquitously found in both bacterial or fungal cell walls and have been implicated in the initiation of anti-microbial immune response. Based on in vitro studies, β-glucans act on several immune receptors including Dectin-1, complement receptor (CR3) and TLR-2/6 and trigger a group of immune cells including macrophages, neutrophils, monocytes, natural killer cells and dendritic cells. As a consequence, both innate and adaptive response can be modulated by β-glucans and they can also enhance opsonic and non-opsonic phagocytosis. In animal studies, after oral administration, the specific backbone 1→3 linear β-glycosidic chain of β-glucans cannot be digested. Most β-glucans enter the proximal small intestine and some are captured by the macrophages. They are internalized and fragmented within the cells, then transported by the macrophages to the marrow and endothelial reticular system. The small β-glucans fragments are eventually released by the macrophages and taken up by other immune cells leading to various immune responses. However, β-glucans of different sizes and branching patterns may have significantly variable immune potency. Careful selection of appropriate β-glucans is essential if we wish to investigate the effects of β-glucans clinically. So far, no good quality clinical trial data is available on assessing the effectiveness of purified β-glucans among cancer patients. Future effort should direct at performing well-designed clinical trials to verify the actual clinical efficacy of β-glucans or β-glucans containing compounds.

/pdf/the-effects-of-b-glucan-on-human-immune-and-cancer-cells-3d1pl05xj2.pdf

The effects of β-glucan on human immune and cancer cells

The diagnostic approach to monogenic very early onset inflammatory bowel disease.

Long-term survival and transplantation of haemopoietic stem cells for immunodeficiencies: report of the European experience 1968–99

Autosomal recessive, complete TYK2 deficiency was previously described in a patient (P1) with intracellular bacterial and viral infections and features of hyper-IgE syndrome (HIES), including atopic dermatitis, high serum IgE levels, and staphylococcal abscesses. We identified seven other TYK2-deficient patients from five families and four different ethnic groups. These patients were homozygous for one of five null mutations, different from that seen in P1. They displayed mycobacterial and/or viral infections, but no HIES. All eight TYK2-deficient patients displayed impaired but not abolished cellular responses to (a) IL-12 and IFN-α/β, accounting for mycobacterial and viral infections, respectively; (b) IL-23, with normal proportions of circulating IL-17+ T cells, accounting for their apparent lack of mucocutaneous candidiasis; and (c) IL-10, with no overt clinical consequences, including a lack of inflammatory bowel disease. Cellular responses to IL-21, IL-27, IFN-γ, IL-28/29 (IFN-λ), and leukemia inhibitory factor (LIF) were normal. The leukocytes and fibroblasts of all seven newly identified TYK2-deficient patients, unlike those of P1, responded normally to IL-6, possibly accounting for the lack of HIES in these patients. The expression of exogenous wild-type TYK2 or the silencing of endogenous TYK2 did not rescue IL-6 hyporesponsiveness, suggesting that this phenotype was not a consequence of the TYK2 genotype. The core clinical phenotype of TYK2 deficiency is mycobacterial and/or viral infections, caused by impaired responses to IL-12 and IFN-α/β. Moreover, impaired IL-6 responses and HIES do not appear to be intrinsic features of TYK2 deficiency in humans.

https://rupress.org/jem/article-pdf/212/10/1641/1213813/jem_20140280.pdf

Human TYK2 deficiency: Mycobacterial and viral infections without hyper-IgE syndrome

Interleukin 10 (IL10) is a key anti-inflammatory cytokine that can inhibit proinflammatory responses of both innate and adaptive immune cells. An association between IL10 and intestinal mucosal homeostasis became clear with the discovery that IL10 and IL10 receptor (IL10R)-deficient mice develop spontaneous intestinal inflammation. Similarly, patients with deleterious mutations in IL10, IL10RA, or IL10RB present with severe enterocolitis within the first months of life. Here, we review recent findings on how IL10- and IL10R-dependent signaling modulates innate and adaptive immune responses in the murine gastrointestinal tract, with implications of their role in the prevention of inflammatory bowel disease (IBD). In addition, we discuss the impact of IL10 and IL10R signaling defects in humans and their relationship to very early-onset IBD (VEO-IBD).

/pdf/interleukin-10-receptor-signaling-master-regulator-of-13wtpubaug.pdf

Interleukin 10 receptor signaling: master regulator of intestinal mucosal homeostasis in mice and humans.

Inflammatory bowel disease is well recognized for a strong genetic involvement in its pathogenesis. Homozygous mutations in interleukin-10 receptor 1 (IL-10R1) identified by linkage analysis were shown to be involved in this disorder. However, the underlying molecular mechanism and the causal nature of the mutations in the disease process remain to be clarified. In this study, using whole exome sequencing, we identified novel compound heterozygous missense mutations in the extracellular domain of IL-10R1 in a Crohn's disease patient from a non-consanguineous family. These mutations did not affect IL-10R1 expression, nor IL-10 binding. However, they abrogated IL-10R1 phosphorylation induced by IL-10, therefore leading to impaired STAT3 activation and suppression of inflammatory responses. After reconstitution with wild-type IL-10R1, the patient cells showed fully restored IL-10R function including IL-10-induced STAT3 activation and expression of suppressor of cytokine signaling 3. Thus, our results demonstrated that the mutations in IL-10R1 extracellular domain impair IL-10R1 activation rather than IL-10 binding, indicating these residues are important in IL-10 signal transduction through IL-10R1. The reconstitution data also confirmed the causality of the IL-10R1 mutations.

Exome sequencing identifies novel compound heterozygous mutations of IL-10 receptor 1 in neonatal-onset Crohn's disease

X-linked agammaglobulinaemia (XLA) is an immunodeficiency caused by Bruton tyrosine kinase (BTK) gene mutations. The disease is characterized by recurrent bacterial infections and profound hypogammaglobulinemia with marked reduction or lack of mature B-cells in the peripheral blood. Molecular characterization of BTK gene provides an opportunity for definitive diagnosis of XLA patients, especially for those with atypical phenotype resulting in a milder or late-onset form of the disease. The diagnosis allows accurate carrier detection with subsequent genetic counselling and prenatal diagnosis. In this study, long polymerase chain reaction (PCR)-direct sequencing analysis of the BTK gene in 12 unrelated Chinese XLA patients had been performed. Eight recurrent mutations and four novel mutations were identified. This is the first report of Chinese cases from three different East Asia regions together, including Hong Kong, Singapore and mainland China. Future clinical and genetic information from the undiagnosed Chinese XLA patients may provide insight into the genotype-phenotype correlations of BTK gene.

Identification of Bruton tyrosine kinase mutations in 12 Chinese patients with X-linked agammaglobulinaemia by long PCR-direct sequencing.

Bone marrow transplantation for primary immunodeficiency diseases

We retrospectively reviewed the clinical characteristics of twenty patients with IgA and/or IgG subclass deficiency attending a tertiary centre. The median age at diagnosis was 1.21 years and the median duration of follow up was 3.83 years. The most common presenting symptom was recurrent sinopulmonary infections (45%). This was followed by refractory asthma (30%), autoimmunity (15%), and other atopic manifestations (10%). Only one out of twenty patients presented with chronic gastrointestinal disease, which contrasted with the majority of previous literature. Three patients had significant pulmonary complications including bronchiolitis obliterans, bronchiectasis and pulmonary fibrosis. The prevalence of IgA deficiency in Hong Kong Chinese population is yet to be established, though it appears not as prevalent as that in western population.

/pdf/review-of-igg-subclass-and-iga-deficiency-in-a-tertiary-1ttc29s3ft.pdf

Review of IgG Subclass and IgA Deficiency in a Tertiary Center

We reviewed retrospectively eleven Chinese children diagnosed with X-linked agammaglobulinaemia (XLA) and managed at the Department of Paediatrics & Adolescent Medicine of Queen Mary Hospital from 1987 to 2002. All of the eleven children had presenting signs and symptoms before fourteen months old, but diagnosis was delayed in most patients with the median age of diagnosis at 5.8 years (range 1.3-14.3 years). The respiratory tract was the most commonly affected site of infection (76%) before diagnosis. Haemophilus influenzae was the most commonly isolated microorganism before and after diagnosis. Intravenous immunoglobulin (IVIG) was given in all patients with a median dose of 700 mg/kg four weekly in order to achieve the pre-infusion IgG level within the normal reference range as well as control of clinical infections. The incidence of documented infections before IVIG replacement was 31 per 100 patient-months which decreased to 7.6 per 100 patient-months after IVIG replacement (p<0.0001). The height and weight centiles of the children also increased after IVIG replacement (p<0.01). Bronchiectasis was noted in three out of the eleven children who were diagnosed to have XLA late at 6, 12 and 14 years old. Adequate IVIG replacement could decrease the frequency of infections and normalize growth in children with XLA. It might prevent bronchiectasis if started early in life, which depends on early diagnosis of XLA.

/pdf/x-linked-agammaglobulinaemia-in-hong-kong-chinese-1tzmn3mib2.pdf

X-linked Agammaglobulinaemia in Hong Kong Chinese

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